PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 29395997-11 2018 Outside of Africa, a single trial suggests a potential role for integrated approaches that combine sulfadoxine-pyrimethamine with azithromycin for IPTp in areas of Papua New Guinea where malaria transmission is high. Azithromycin 130-142 tRNA isopentenyltransferase 1 Homo sapiens 147-151 29384912-5 2017 Interestingly, the alanine aminotransferase level (ALT) reached 211.2 U/L on day 9 after azithromycin administration. Azithromycin 89-101 glutamic--pyruvic transaminase Homo sapiens 19-43 29874670-1 2018 AIMS: The purpose of this paper was to determine the lacrimal concentration of IL-1alpha and MMP-9 in patients with active ocular rosacea before and after systemic treatment with azithromycin or doxycycline. Azithromycin 179-191 interleukin 1 alpha Homo sapiens 79-88 29874670-1 2018 AIMS: The purpose of this paper was to determine the lacrimal concentration of IL-1alpha and MMP-9 in patients with active ocular rosacea before and after systemic treatment with azithromycin or doxycycline. Azithromycin 179-191 matrix metallopeptidase 9 Homo sapiens 93-98 29874670-4 2018 IL-1alpha decreased from 47.0 pg/mL before azithromycin to 23.5 pg/mL after treatment (p = 0.024), but not after doxycycline therapy. Azithromycin 43-55 interleukin 1 alpha Homo sapiens 0-9 29874670-7 2018 Patients unresponsive to azithromycin had significantly higher baseline MMP-9 levels than those with doxycycline (p = 0.040). Azithromycin 25-37 matrix metallopeptidase 9 Homo sapiens 72-77 29874670-8 2018 CONCLUSIONS: While IL-1alpha levels decreased after azithromycin therapy, MMP-9 did so after doxycycline treatment. Azithromycin 52-64 interleukin 1 alpha Homo sapiens 19-28 29289941-0 2017 Azithromycin to prevent post-discharge morbidity and mortality in Kenyan children: a protocol for a randomised, double-blind, placebo-controlled trial (the Toto Bora trial). Azithromycin 0-12 HOP homeobox Homo sapiens 156-160 29535704-12 2018 Resistance to the antibiotics was presumably given by ermF, carA and msrA for azithromycin, mutations of the gyrA and grlB for norfloxacin, and by sul123 genes for sulfamethoxazole. Azithromycin 78-90 methionine sulfoxide reductase A Homo sapiens 69-73 31011342-6 2018 The best azithromycin removal conditions were obtained at the removal efficiency with the initial concentration of antibiotic 5 mgL-1, the concentration of persulfate 1mmol, and the contact time 30 min. Azithromycin 9-21 LLGL scribble cell polarity complex component 1 Homo sapiens 128-133 28684545-6 2017 Plasma IL-18 levels were determined from patients who were diagnosed with bronchiectasis isolated with or without P. aeruginosa and treated with azithromycin for 3-5 days. Azithromycin 145-157 interleukin 18 Homo sapiens 7-12 29098024-9 2017 AZM also down-regulated the concentration and mRNA expression of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and transforming growth factor-beta1. Azithromycin 0-3 interleukin 1 beta Mus musculus 65-87 29098024-9 2017 AZM also down-regulated the concentration and mRNA expression of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and transforming growth factor-beta1. Azithromycin 0-3 interleukin 6 Mus musculus 89-93 29098024-9 2017 AZM also down-regulated the concentration and mRNA expression of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and transforming growth factor-beta1. Azithromycin 0-3 tumor necrosis factor Mus musculus 95-159 29098024-10 2017 In addition, AZM attenuated the irradiation-induced increases in the mRNA expression of fibrotic markers (alpha-smooth muscle actin and alpha-1 type I collagen). Azithromycin 13-16 collagen, type I, alpha 1 Mus musculus 136-159 28684545-7 2017 Azithromycin treatment enhanced bacterial clearance and attenuated lung injury in mice chronically infected with P. aeruginosa, which resulted from the inhibition of caspase-1-dependent IL-1beta and IL-18 secretion. Azithromycin 0-12 interleukin 18 Homo sapiens 199-204 28684545-10 2017 Azithromycin administration markedly decreased IL-18 secretion in bronchiectasis patients. Azithromycin 0-12 interleukin 18 Homo sapiens 47-52 28861888-14 2017 The level of serum IL-17 in the azithromycin + Qingfei Mixture treatment group was lower than that in the azithromycin or Qingfei Mixture groups (P<0.01). Azithromycin 32-44 interleukin 17A Rattus norvegicus 19-24 28664473-8 2017 The expression levels of VEGF, IL-6, and IL-10 also decreased in response to treatment with QTF or AZM. Azithromycin 99-102 vascular endothelial growth factor A Homo sapiens 25-29 28664473-8 2017 The expression levels of VEGF, IL-6, and IL-10 also decreased in response to treatment with QTF or AZM. Azithromycin 99-102 interleukin 6 Homo sapiens 31-35 28664473-8 2017 The expression levels of VEGF, IL-6, and IL-10 also decreased in response to treatment with QTF or AZM. Azithromycin 99-102 interleukin 10 Homo sapiens 41-46 28861888-14 2017 The level of serum IL-17 in the azithromycin + Qingfei Mixture treatment group was lower than that in the azithromycin or Qingfei Mixture groups (P<0.01). Azithromycin 106-118 interleukin 17A Rattus norvegicus 19-24 28479141-6 2017 Thereby, azithromycin altered tropomyosin-related kinase A (TrkA) signaling and attenuated protein kinase B (Akt) activity, which subsequently induced autophagy. Azithromycin 9-21 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 30-58 28885357-10 2017 However, patients in the azithromycin group had longer time to defervescence (mean difference 4.38 hours, 95% CI -2.51 to 11.27) and higher rate of fever for more than 48 hours (RR 1.31, 95% CI 0.81-2.12). Azithromycin 25-37 ribonucleotide reductase catalytic subunit M1 Homo sapiens 178-182 28479141-6 2017 Thereby, azithromycin altered tropomyosin-related kinase A (TrkA) signaling and attenuated protein kinase B (Akt) activity, which subsequently induced autophagy. Azithromycin 9-21 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 60-64 28479141-6 2017 Thereby, azithromycin altered tropomyosin-related kinase A (TrkA) signaling and attenuated protein kinase B (Akt) activity, which subsequently induced autophagy. Azithromycin 9-21 AKT serine/threonine kinase 1 Rattus norvegicus 109-112 28817779-10 2017 The average price difference within a zip code was $52 for levofloxacin and $17 for azithromycin. Azithromycin 84-96 death associated protein kinase 3 Homo sapiens 38-41 28535933-11 2017 Additional ex vivo studies confirmed reduced induction of IL-6 (P = 0.017) and CXCL8/IL-8 (P = 0.005) with azithromycin. Azithromycin 107-119 interleukin 6 Homo sapiens 58-62 28535933-11 2017 Additional ex vivo studies confirmed reduced induction of IL-6 (P = 0.017) and CXCL8/IL-8 (P = 0.005) with azithromycin. Azithromycin 107-119 C-X-C motif chemokine ligand 8 Homo sapiens 79-84 28535933-11 2017 Additional ex vivo studies confirmed reduced induction of IL-6 (P = 0.017) and CXCL8/IL-8 (P = 0.005) with azithromycin. Azithromycin 107-119 C-X-C motif chemokine ligand 8 Homo sapiens 85-89 28613983-0 2017 Azithromycin attenuates myofibroblast differentiation and lung fibrosis development through proteasomal degradation of NOX4. Azithromycin 0-12 NADPH oxidase 4 Homo sapiens 119-123 28613983-4 2017 Hence, we hypothesized that AZM may regulate NOX4 levels by modulating proteostasis machineries, resulting in inhibition of TGFB-associated lung fibrosis development. Azithromycin 28-31 NADPH oxidase 4 Homo sapiens 45-49 28613983-4 2017 Hence, we hypothesized that AZM may regulate NOX4 levels by modulating proteostasis machineries, resulting in inhibition of TGFB-associated lung fibrosis development. Azithromycin 28-31 transforming growth factor beta 1 Homo sapiens 124-128 28613983-8 2017 TGFB-induced NOX4 and myofibroblast differentiation were clearly inhibited by AZM treatment in LF. Azithromycin 78-81 transforming growth factor beta 1 Homo sapiens 0-4 28613983-8 2017 TGFB-induced NOX4 and myofibroblast differentiation were clearly inhibited by AZM treatment in LF. Azithromycin 78-81 NADPH oxidase 4 Homo sapiens 13-17 28613983-9 2017 AZM-mediated NOX4 reduction was restored by treatment with MG132, a proteasome inhibitor. Azithromycin 0-3 NADPH oxidase 4 Homo sapiens 13-17 28613983-11 2017 Autophagy inhibition by AZM was linked to ubiquitination of NOX4 via increased protein levels of STUB1 (STIP1 homology and U-box containing protein 1), an E3 ubiquitin ligase. Azithromycin 24-27 NADPH oxidase 4 Homo sapiens 60-64 28613983-11 2017 Autophagy inhibition by AZM was linked to ubiquitination of NOX4 via increased protein levels of STUB1 (STIP1 homology and U-box containing protein 1), an E3 ubiquitin ligase. Azithromycin 24-27 STIP1 homology and U-box containing protein 1 Homo sapiens 97-102 28613983-11 2017 Autophagy inhibition by AZM was linked to ubiquitination of NOX4 via increased protein levels of STUB1 (STIP1 homology and U-box containing protein 1), an E3 ubiquitin ligase. Azithromycin 24-27 stress induced phosphoprotein 1 Homo sapiens 104-109 28613983-13 2017 AZM suppressed lung fibrosis development induced by BLM with concomitantly reduced NOX4 protein levels and enhanced proteasome activation. Azithromycin 0-3 NADPH oxidase 4 Homo sapiens 83-87 28613983-14 2017 These results suggest that AZM suppresses NOX4 by promoting proteasomal degradation, resulting in inhibition of TGFB-induced myofibroblast differentiation and lung fibrosis development. Azithromycin 27-30 NADPH oxidase 4 Homo sapiens 42-46 28613983-14 2017 These results suggest that AZM suppresses NOX4 by promoting proteasomal degradation, resulting in inhibition of TGFB-induced myofibroblast differentiation and lung fibrosis development. Azithromycin 27-30 transforming growth factor beta 1 Homo sapiens 112-116 28759625-3 2017 METHODS: TNF-alpha was measured from supernatants of RAW 264.7 cells stimulated with GBS isolates, in presence of four treatment regimens: ampicillin alone, azithromycin alone, or combination of azithromycin plus ampicillin. Azithromycin 195-207 tumor necrosis factor Mus musculus 9-18 28759625-6 2017 RESULTS: GBS isolates exposed to azithromycin or combination (compared to ampicillin alone) stimulated less TNF production in vitro. Azithromycin 33-45 tumor necrosis factor Mus musculus 108-111 28759625-8 2017 Mean serum IL-6 was lower in mice treated with azithromycin alone (66+-52 pg/ml) or combination of ampicillin plus azithromycin (52+-22 pg/ml) compared to ampicillin alone (260+-160 pg/ml) (p<0.005). Azithromycin 47-59 interleukin 6 Mus musculus 11-15 28759625-8 2017 Mean serum IL-6 was lower in mice treated with azithromycin alone (66+-52 pg/ml) or combination of ampicillin plus azithromycin (52+-22 pg/ml) compared to ampicillin alone (260+-160 pg/ml) (p<0.005). Azithromycin 115-127 interleukin 6 Mus musculus 11-15 28659178-0 2017 Azithromycin decreases NALP3 mRNA stability in monocytes to limit inflammasome-dependent inflammation. Azithromycin 0-12 NLR family pyrin domain containing 3 Homo sapiens 23-28 28693139-0 2017 Azithromycin effectively inhibits tumor angiogenesis by suppressing vascular endothelial growth factor receptor 2-mediated signaling pathways in lung cancer. Azithromycin 0-12 kinase insert domain receptor Homo sapiens 68-113 28659178-2 2017 Azithromycin inhibits IL-1beta-mediated inflammation that is dependent, in part, on inflammasome activity. Azithromycin 0-12 interleukin 1 beta Homo sapiens 22-30 28693139-5 2017 In addition, azithromycin induces apoptosis of HLT-ECs even in the presence of VEGF. Azithromycin 13-25 vascular endothelial growth factor A Homo sapiens 79-83 28693139-8 2017 Notably, the inhibitory effects of azithromycin on angiogenesis are associated with its ability to suppress VEGF-induced activation of VEGF receptor 2 (VEGFR2), phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), focal adhesion kinase, and disruption of focal adhesion assembly and actin stress fiber formation in HLT-ECs. Azithromycin 35-47 vascular endothelial growth factor A Homo sapiens 108-112 28693139-8 2017 Notably, the inhibitory effects of azithromycin on angiogenesis are associated with its ability to suppress VEGF-induced activation of VEGF receptor 2 (VEGFR2), phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), focal adhesion kinase, and disruption of focal adhesion assembly and actin stress fiber formation in HLT-ECs. Azithromycin 35-47 kinase insert domain receptor Homo sapiens 135-150 28693139-8 2017 Notably, the inhibitory effects of azithromycin on angiogenesis are associated with its ability to suppress VEGF-induced activation of VEGF receptor 2 (VEGFR2), phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), focal adhesion kinase, and disruption of focal adhesion assembly and actin stress fiber formation in HLT-ECs. Azithromycin 35-47 kinase insert domain receptor Homo sapiens 152-158 28693139-8 2017 Notably, the inhibitory effects of azithromycin on angiogenesis are associated with its ability to suppress VEGF-induced activation of VEGF receptor 2 (VEGFR2), phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), focal adhesion kinase, and disruption of focal adhesion assembly and actin stress fiber formation in HLT-ECs. Azithromycin 35-47 AKT serine/threonine kinase 1 Homo sapiens 212-215 28693139-9 2017 The present study identifies that azithromycin targets VEGFR2-mediated focal adhesion and PI3K/Akt signaling pathways in HLT-ECs, leading to the suppression of angiogenesis and lung tumor growth. Azithromycin 34-46 kinase insert domain receptor Homo sapiens 55-61 28693139-9 2017 The present study identifies that azithromycin targets VEGFR2-mediated focal adhesion and PI3K/Akt signaling pathways in HLT-ECs, leading to the suppression of angiogenesis and lung tumor growth. Azithromycin 34-46 AKT serine/threonine kinase 1 Homo sapiens 95-98 28659178-3 2017 Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes. Azithromycin 37-49 NLR family pyrin domain containing 3 Homo sapiens 57-105 28638254-9 2017 Twenty-three of the patients were treated with azithromycin, and they had more severe clinical and radiological parameters than those who were not but nevertheless presented significantly lower levels of TNF-alpha. Azithromycin 47-59 tumor necrosis factor Homo sapiens 204-213 28659178-3 2017 Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes. Azithromycin 37-49 NLR family pyrin domain containing 3 Homo sapiens 107-112 28659178-3 2017 Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes. Azithromycin 37-49 NLR family pyrin domain containing 3 Homo sapiens 161-166 28659178-4 2017 METHODS: THP-1 cells were treated with azithromycin alone, LPS alone, or both. Azithromycin 39-51 GLI family zinc finger 2 Homo sapiens 9-14 28659178-8 2017 THP-1 Lucia cells which contain an NF-kappaB responsive luciferase element were used to assess NF-kappaB activity in response to azithromycin, LPS, and azithromycin/LPS by measuring luminescence. Azithromycin 129-141 GLI family zinc finger 2 Homo sapiens 0-5 28659178-8 2017 THP-1 Lucia cells which contain an NF-kappaB responsive luciferase element were used to assess NF-kappaB activity in response to azithromycin, LPS, and azithromycin/LPS by measuring luminescence. Azithromycin 152-164 GLI family zinc finger 2 Homo sapiens 0-5 28659178-9 2017 To confirm azithromycin"s effects on NLRP3 mRNA and promoter activity conclusively, HEK cells were lipofected with luciferase reporter constructs harboring either the 5" untranslated region (UTR) of the NLRP3 gene which included the promoter, the 3" UTR of the gene, or an empty plasmid prior to treatment with azithromycin and/or LPS, and luminescence was measured. Azithromycin 11-23 NLR family pyrin domain containing 3 Homo sapiens 37-42 28659178-10 2017 RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity. Azithromycin 9-21 interleukin 1 beta Homo sapiens 32-40 28659178-10 2017 RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity. Azithromycin 9-21 NLR family pyrin domain containing 3 Homo sapiens 60-65 28659178-10 2017 RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity. Azithromycin 9-21 GLI family zinc finger 2 Homo sapiens 99-104 28659178-10 2017 RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity. Azithromycin 9-21 NLR family pyrin domain containing 3 Homo sapiens 177-182 28659178-10 2017 RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity. Azithromycin 9-21 NLR family pyrin domain containing 3 Homo sapiens 192-197 28659178-12 2017 CONCLUSIONS: These studies provide a unique mechanism whereby azithromycin exerts immunomodulatory actions in monocytes by destabilizing mRNA levels for a key inflammasome component, NALP3, leading to decreased IL-1beta-mediated inflammation. Azithromycin 62-74 NLR family pyrin domain containing 3 Homo sapiens 183-188 28659178-12 2017 CONCLUSIONS: These studies provide a unique mechanism whereby azithromycin exerts immunomodulatory actions in monocytes by destabilizing mRNA levels for a key inflammasome component, NALP3, leading to decreased IL-1beta-mediated inflammation. Azithromycin 62-74 interleukin 1 beta Homo sapiens 211-219 28638254-12 2017 The use of azithromycin was associated with reduced TNF-alpha levels and did not influence oxidation parameters. Azithromycin 11-23 tumor necrosis factor Homo sapiens 52-61 28415826-0 2017 Azithromycin augments rhinovirus-induced IFNbeta via cytosolic MDA5 in experimental models of asthma exacerbation. Azithromycin 0-12 interferon beta 1, fibroblast Mus musculus 41-48 28415826-0 2017 Azithromycin augments rhinovirus-induced IFNbeta via cytosolic MDA5 in experimental models of asthma exacerbation. Azithromycin 0-12 interferon induced with helicase C domain 1 Mus musculus 63-67 28415826-4 2017 Here, we investigated if azithromycin induces IFNbeta expression in vitro in rhinovirus-infected bronchial epithelial cells from asthmatic donors and in vivo in our allergic inflammation-based mouse model of viral stimulus-induced asthma exacerbations. Azithromycin 25-37 interferon beta 1, fibroblast Mus musculus 46-53 28415826-5 2017 Azithromycin dose-dependently augmented viral-induced IFNbeta expression in asthmatic, but not in healthy bronchial epithelial cells. Azithromycin 0-12 interferon beta 1, fibroblast Mus musculus 54-61 28415826-8 2017 In vivo azithromycin induced IFNbeta protein, restoring a reduced lung IFN response exclusively in allergic exacerbating mice. Azithromycin 8-20 interferon beta 1, fibroblast Mus musculus 29-36 28415826-10 2017 We suggest that clinically relevant concentrations of azithromycin produce MDA5-dependent, anti-viral, IFN-inducing effects in bronchial epithelium distinctly from asthmatic donors. Azithromycin 54-66 interferon induced with helicase C domain 1 Mus musculus 75-79 28415826-11 2017 Similarly, azithromycin induced MDA5-associated IFN in virally stimulated lungs in vivo exclusively in allergic mice. Azithromycin 11-23 interferon induced with helicase C domain 1 Mus musculus 32-36 27916734-2 2017 In the present study, we hypothesized that azithromycin alleviated airway epithelium injury through inhibiting airway epithelium apoptosis via down regulation of caspase-3 and Bax/Bcl2 ratio in vivo and in vitro. Azithromycin 43-55 caspase 3 Homo sapiens 162-171 28436019-17 2017 In a sensitivity analysis limited to a single study at low risk of bias, azithromycin was superior to doxycycline in achieving cure in mild-moderate PID (RR 1.35, 95% CI 1.10 to 1.67, 133 women, moderate-quality evidence). Azithromycin 73-85 metastasis associated 1 family member 2 Homo sapiens 149-152 28436019-24 2017 Moderate-quality evidence from a single study at low risk of bias suggested that a macrolide (azithromycin) may be more effective than a tetracycline (doxycycline) for curing mild-moderate PID. Azithromycin 94-106 metastasis associated 1 family member 2 Homo sapiens 189-192 28356719-4 2017 The AZT-resistance genes (ermA, ermB, ermC, mefA, and msrA) were identified in the resistant strains using quantitative polymerase chain reaction. Azithromycin 4-7 rRNA methylase Erm(A) Staphylococcus aureus 26-30 28356719-4 2017 The AZT-resistance genes (ermA, ermB, ermC, mefA, and msrA) were identified in the resistant strains using quantitative polymerase chain reaction. Azithromycin 4-7 ABC transporter permease protein Staphylococcus aureus 54-58 28240815-4 2017 This is achieved by the immobilization of the antibiotic azithromycin into the membrane via a solvent evaporation technique leading to a sustained release of the drug over 14 d. In vitro testing shows that this controlled release of azithromycin is proficient at inhibiting the growth of Staphylococcus aureus for 14 d. Implantation of azithromycin loaded mPCL membrane in a rodent calvarial defect induces macrophage polarization toward the M2 phenotype after one week and results in significantly more bone regeneration eight weeks post-surgery. Azithromycin 57-69 polycystic kidney disease 2-like 1 Mus musculus 356-360 28240815-4 2017 This is achieved by the immobilization of the antibiotic azithromycin into the membrane via a solvent evaporation technique leading to a sustained release of the drug over 14 d. In vitro testing shows that this controlled release of azithromycin is proficient at inhibiting the growth of Staphylococcus aureus for 14 d. Implantation of azithromycin loaded mPCL membrane in a rodent calvarial defect induces macrophage polarization toward the M2 phenotype after one week and results in significantly more bone regeneration eight weeks post-surgery. Azithromycin 233-245 polycystic kidney disease 2-like 1 Mus musculus 356-360 28240815-4 2017 This is achieved by the immobilization of the antibiotic azithromycin into the membrane via a solvent evaporation technique leading to a sustained release of the drug over 14 d. In vitro testing shows that this controlled release of azithromycin is proficient at inhibiting the growth of Staphylococcus aureus for 14 d. Implantation of azithromycin loaded mPCL membrane in a rodent calvarial defect induces macrophage polarization toward the M2 phenotype after one week and results in significantly more bone regeneration eight weeks post-surgery. Azithromycin 233-245 polycystic kidney disease 2-like 1 Mus musculus 356-360 28369077-0 2017 Differential inhibition of activity, activation and gene expression of MMP-9 in THP-1 cells by azithromycin and minocycline versus bortezomib: A comparative study. Azithromycin 95-107 matrix metallopeptidase 9 Homo sapiens 71-76 28369077-7 2017 In a considerable set of recent publications, two antibiotics (minocycline and azythromycin) and the proteasome inhibitor bortezomib, used in cancers, were reported to inhibit MMP-9 at different stages of its expression, activation or activity. Azithromycin 79-91 matrix metallopeptidase 9 Homo sapiens 176-181 28369077-10 2017 In contrast, azithromycin specifically reduced MMP-9 mRNA and protein levels without affecting NF-kappaB in endotoxin-challenged monocytic THP-1 cells. Azithromycin 13-25 matrix metallopeptidase 9 Homo sapiens 47-52 28369077-12 2017 Overall, our study clarified that azithromycin decreased the levels of MMP-9 by reduction of gene and protein expression while minocycline inhibits proteolytic activity at high concentrations. Azithromycin 34-46 matrix metallopeptidase 9 Homo sapiens 71-76 28408648-6 2017 Acute exposure to azithromycin reduced peak SCN5A currents in HEK cells (IC50=110+-3 mumol/L) and Na+ current in mouse ventricular myocytes. Azithromycin 18-30 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-49 28408648-7 2017 However, with chronic (24 hour) exposure, azithromycin caused a 2-fold increase in both peak and late SCN5A currents, with findings confirmed for INa in cardiomyocytes. Azithromycin 42-54 sodium voltage-gated channel alpha subunit 5 Homo sapiens 103-108 28078769-2 2017 Persistently elevated BAL-neutrophilia is observed in some patients despite treatment with azithromycin, which may be induced by IL-1alpha. Azithromycin 91-103 interleukin 1 alpha Homo sapiens 129-138 28400764-9 2017 Besides, mphA gene was identified in 15 of the 31 azithromycin-resistant isolates. Azithromycin 50-62 macrolide 2'-phosphotransferase I Salmonella enterica subsp. enterica serovar Typhimurium 9-13 27916734-11 2017 SIGNIFICANCE: Azithromycin is an attractive treatment option for reducing airway epithelial cell apoptosis by improving the imbalance of Bax/Bcl-2 ratio and inhibiting Caspase-3 level in airway epithelium. Azithromycin 14-26 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 27916734-11 2017 SIGNIFICANCE: Azithromycin is an attractive treatment option for reducing airway epithelial cell apoptosis by improving the imbalance of Bax/Bcl-2 ratio and inhibiting Caspase-3 level in airway epithelium. Azithromycin 14-26 BCL2 apoptosis regulator Homo sapiens 141-146 27916734-11 2017 SIGNIFICANCE: Azithromycin is an attractive treatment option for reducing airway epithelial cell apoptosis by improving the imbalance of Bax/Bcl-2 ratio and inhibiting Caspase-3 level in airway epithelium. Azithromycin 14-26 caspase 3 Homo sapiens 168-177 27916734-2 2017 In the present study, we hypothesized that azithromycin alleviated airway epithelium injury through inhibiting airway epithelium apoptosis via down regulation of caspase-3 and Bax/Bcl2 ratio in vivo and in vitro. Azithromycin 43-55 BCL2 associated X, apoptosis regulator Homo sapiens 176-179 27916734-2 2017 In the present study, we hypothesized that azithromycin alleviated airway epithelium injury through inhibiting airway epithelium apoptosis via down regulation of caspase-3 and Bax/Bcl2 ratio in vivo and in vitro. Azithromycin 43-55 BCL2 apoptosis regulator Homo sapiens 180-184 27916734-9 2017 Moreover, the increasing mRNA and protein expressions of Caspase-3 and Bax/Bcl-2 ratio in lung tissue were all significantly decreased in azithromycin-treated rats (P<0.05). Azithromycin 138-150 caspase 3 Rattus norvegicus 57-66 27916734-9 2017 Moreover, the increasing mRNA and protein expressions of Caspase-3 and Bax/Bcl-2 ratio in lung tissue were all significantly decreased in azithromycin-treated rats (P<0.05). Azithromycin 138-150 BCL2 associated X, apoptosis regulator Rattus norvegicus 71-74 27916734-9 2017 Moreover, the increasing mRNA and protein expressions of Caspase-3 and Bax/Bcl-2 ratio in lung tissue were all significantly decreased in azithromycin-treated rats (P<0.05). Azithromycin 138-150 BCL2, apoptosis regulator Rattus norvegicus 75-80 27916734-10 2017 In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05). Azithromycin 10-22 transforming growth factor beta 1 Homo sapiens 48-57 27916734-10 2017 In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05). Azithromycin 10-22 transforming growth factor beta 1 Homo sapiens 115-124 27916734-10 2017 In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05). Azithromycin 10-22 caspase 3 Homo sapiens 134-143 27916734-10 2017 In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05). Azithromycin 10-22 BCL2 associated X, apoptosis regulator Homo sapiens 159-162 27916734-10 2017 In vitro, azithromycin significantly suppressed TGF-beta1-induced BEAS-2B cells apoptosis (P<0.05) and reversed TGF-beta1 elevated Caspase-3 mRNA level and Bax/Bcl-2 ratio (P<0.05). Azithromycin 10-22 BCL2 apoptosis regulator Homo sapiens 163-168 29441859-7 2017 Moreover, E-cadherin and vimentin expressions were more positive in the IM and AZM group than in the other groups. Azithromycin 79-82 cadherin 1 Homo sapiens 10-20 28598854-9 2017 Co-administration of AZM and a previously developed antisense oligonucleotide that increases SMN2 splicing, resulted in an improvement in the SMA phenotype beyond either AZM or ASO alone, including a highly significant extension in survival with improvement in body weight and movement. Azithromycin 21-24 glutamate receptor, metabotropic 7 Mus musculus 93-97 29441859-7 2017 Moreover, E-cadherin and vimentin expressions were more positive in the IM and AZM group than in the other groups. Azithromycin 79-82 vimentin Homo sapiens 25-33 28738346-8 2017 In the infection model, the mice survival were increased markedly, the inflammations of infected lungs were improved greatly along with reduced IL-6, IL-8 and ascended IL-10 at 0.8 mg/kg of AZM combined with 3.2 mg/kg of BER. Azithromycin 190-193 interleukin 6 Mus musculus 144-148 28738346-8 2017 In the infection model, the mice survival were increased markedly, the inflammations of infected lungs were improved greatly along with reduced IL-6, IL-8 and ascended IL-10 at 0.8 mg/kg of AZM combined with 3.2 mg/kg of BER. Azithromycin 190-193 interleukin 10 Mus musculus 168-173 28219060-7 2017 Plasma TNFalpha (total) concentrations in azithromycin/prednisolone patients were significantly higher than those in WAT patients and similar to those of healthy children. Azithromycin 42-54 tumor necrosis factor Homo sapiens 7-15 28219060-8 2017 In contrast, IL-10 (total) levels were significantly decreased in azithromycin/prednisolone-treated patients compared with WAT patients. Azithromycin 66-78 interleukin 10 Homo sapiens 13-18 28219060-9 2017 Children from the azithromycin group demonstrated ACTH levels similar to those of healthy controls. Azithromycin 18-30 proopiomelanocortin Homo sapiens 50-54 28598854-9 2017 Co-administration of AZM and a previously developed antisense oligonucleotide that increases SMN2 splicing, resulted in an improvement in the SMA phenotype beyond either AZM or ASO alone, including a highly significant extension in survival with improvement in body weight and movement. Azithromycin 170-173 glutamate receptor, metabotropic 7 Mus musculus 93-97 27825282-0 2016 Relationship between maternal c-reactive protein level and neonatal outcome in patients with preterm premature rupture of membranes treated with Ampicillin and Azithromycin. Azithromycin 160-172 C-reactive protein Homo sapiens 30-48 27486204-9 2017 Compared with placebo, AZM treatment led to reduced in-vivo levels of chemokine (C-X-C) ligand 1 (CXCL1), tumour necrosis factor (TNF)-alpha, interleukin (IL)-13 and IL-12p40 in BAL, but increased bacterial metabolites including glycolic acid, indol-3-acetate and linoleic acid. Azithromycin 23-26 C-X-C motif chemokine ligand 1 Homo sapiens 98-103 27486204-9 2017 Compared with placebo, AZM treatment led to reduced in-vivo levels of chemokine (C-X-C) ligand 1 (CXCL1), tumour necrosis factor (TNF)-alpha, interleukin (IL)-13 and IL-12p40 in BAL, but increased bacterial metabolites including glycolic acid, indol-3-acetate and linoleic acid. Azithromycin 23-26 tumor necrosis factor Homo sapiens 106-140 27977675-6 2016 AZM and CAM induced cell death under the amino acid-depleted (AAD) culture condition in these cell lines along with CHOP upregulation, although they showed no cytotoxicity under the complete culture medium. Azithromycin 0-3 DNA-damage inducible transcript 3 Mus musculus 116-120 27977675-8 2016 CHOP-/- murine embryonic fibroblast (MEF) cell lines also attenuated AZM-induced cell death compared with CHOP+/+ MEF cell lines. Azithromycin 69-72 DNA-damage inducible transcript 3 Mus musculus 0-4 27653939-4 2016 Design, Setting, and Participants: The Azithromycin Against Placebo in Exacerbations of Asthma (AZALEA) randomized, double-blind, placebo-controlled clinical trial, a United Kingdom-based multicenter study in adults requesting emergency care for acute asthma exacerbations, ran from September 2011 to April 2014. Azithromycin 39-51 RAN, member RAS oncogene family Homo sapiens 104-107 28283010-16 2017 IL-12 and IFN-gamma levels were highest in IC group and the lowest in AZT + CV group. Azithromycin 70-73 interferon gamma Mus musculus 10-19 28283010-18 2017 IL-2 levels were significantly higher in CV, CV + AZT groups than in the other groups (p< 0.001). Azithromycin 50-53 interleukin 2 Mus musculus 0-4 27895643-7 2016 Azithromycin attenuated the responses, mainly of macrophage chemoattractant protein-1, tumor necrosis factor-alpha, and interferon-gamma, in CF but not in wild-type mice. Azithromycin 0-12 tumor necrosis factor Mus musculus 76-114 27895643-7 2016 Azithromycin attenuated the responses, mainly of macrophage chemoattractant protein-1, tumor necrosis factor-alpha, and interferon-gamma, in CF but not in wild-type mice. Azithromycin 0-12 interferon gamma Mus musculus 120-136 27664570-0 2016 Azithromycin modulates immune response of human monocyte-derived dendritic cells and CD4+ T cells. Azithromycin 0-12 CD4 molecule Homo sapiens 85-88 27664570-2 2016 In the present study, we investigated the ability of AZM to influence the function of human monocyte-derived dendritic cells (DCs) and CD4+ T cells. Azithromycin 53-56 CD4 molecule Homo sapiens 135-138 27664570-3 2016 We found that AZM down-regulated CD80, CD86, and HLA-DR expression in lipopolysaccharide (LPS)-stimulated DCs and suppressed interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-alpha production in these cells. Azithromycin 14-17 CD80 molecule Homo sapiens 33-37 27664570-3 2016 We found that AZM down-regulated CD80, CD86, and HLA-DR expression in lipopolysaccharide (LPS)-stimulated DCs and suppressed interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-alpha production in these cells. Azithromycin 14-17 CD86 molecule Homo sapiens 39-43 27664570-3 2016 We found that AZM down-regulated CD80, CD86, and HLA-DR expression in lipopolysaccharide (LPS)-stimulated DCs and suppressed interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-alpha production in these cells. Azithromycin 14-17 interleukin 6 Homo sapiens 125-143 27664570-3 2016 We found that AZM down-regulated CD80, CD86, and HLA-DR expression in lipopolysaccharide (LPS)-stimulated DCs and suppressed interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-alpha production in these cells. Azithromycin 14-17 interleukin 10 Homo sapiens 145-150 27664570-3 2016 We found that AZM down-regulated CD80, CD86, and HLA-DR expression in lipopolysaccharide (LPS)-stimulated DCs and suppressed interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-alpha production in these cells. Azithromycin 14-17 tumor necrosis factor Homo sapiens 163-190 27664570-4 2016 In addition, AZM increased endocytosis and/or expression of Toll-like receptor (TLR)2, TLR4, and TLR9 in DCs and suppressed anti-CD3/CD28-induced CD4+ T cell proliferation and interferon-gamma production, an effect that was synergistic with dexamethasone. Azithromycin 13-16 toll like receptor 2 Homo sapiens 80-85 27664570-4 2016 In addition, AZM increased endocytosis and/or expression of Toll-like receptor (TLR)2, TLR4, and TLR9 in DCs and suppressed anti-CD3/CD28-induced CD4+ T cell proliferation and interferon-gamma production, an effect that was synergistic with dexamethasone. Azithromycin 13-16 toll like receptor 4 Homo sapiens 87-91 27664570-4 2016 In addition, AZM increased endocytosis and/or expression of Toll-like receptor (TLR)2, TLR4, and TLR9 in DCs and suppressed anti-CD3/CD28-induced CD4+ T cell proliferation and interferon-gamma production, an effect that was synergistic with dexamethasone. Azithromycin 13-16 toll like receptor 9 Homo sapiens 97-101 27664570-4 2016 In addition, AZM increased endocytosis and/or expression of Toll-like receptor (TLR)2, TLR4, and TLR9 in DCs and suppressed anti-CD3/CD28-induced CD4+ T cell proliferation and interferon-gamma production, an effect that was synergistic with dexamethasone. Azithromycin 13-16 CD4 molecule Homo sapiens 146-149 27664570-4 2016 In addition, AZM increased endocytosis and/or expression of Toll-like receptor (TLR)2, TLR4, and TLR9 in DCs and suppressed anti-CD3/CD28-induced CD4+ T cell proliferation and interferon-gamma production, an effect that was synergistic with dexamethasone. Azithromycin 13-16 interferon gamma Homo sapiens 176-192 27664570-6 2016 Our study demonstrates that AZM modulates DC and CD4+ T cell function and may be of therapeutic benefit in various inflammatory disorders. Azithromycin 28-31 CD4 molecule Homo sapiens 49-52 27449383-0 2016 Azithromycin impairs TLR7 signaling in dendritic cells and improves the severity of imiquimod-induced psoriasis-like skin inflammation in mice. Azithromycin 0-12 toll-like receptor 7 Mus musculus 21-25 27449383-2 2016 The macrolide antibiotic azithromycin (AZM) had been demonstrated to inhibit the TLR4 agonist-induced maturation and activation of murine bone marrow-derived DCs (BMDCs). Azithromycin 25-37 toll-like receptor 4 Mus musculus 81-85 27449383-2 2016 The macrolide antibiotic azithromycin (AZM) had been demonstrated to inhibit the TLR4 agonist-induced maturation and activation of murine bone marrow-derived DCs (BMDCs). Azithromycin 39-42 toll-like receptor 4 Mus musculus 81-85 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 CD40 antigen Mus musculus 81-85 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 CD80 antigen Mus musculus 90-94 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 tumor necrosis factor Mus musculus 108-117 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 interleukin 10 Mus musculus 119-124 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 interleukin 12b Mus musculus 126-134 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 interleukin 23, alpha subunit p19 Mus musculus 146-154 27449383-7 2016 RESULTS: AZM significantly inhibited the expression of co-stimulatory molecules (CD40 and CD80) and reduced TNF-alpha, IL-10, IL-12p40, IL-12p70, IL-23p19 in BMDCs and IFN-alpha production in plasmacytoid DCs. Azithromycin 9-12 interferon alpha Mus musculus 168-177 27449383-8 2016 AZM treatment impaired lysosomal acidification, interrupted TLR7 maturation in the lysosome, and ultimately blocked the IMQ-induced NF-kappaB and IRF-7 nuclear translocation in DCs. Azithromycin 0-3 toll-like receptor 7 Mus musculus 60-64 27449383-8 2016 AZM treatment impaired lysosomal acidification, interrupted TLR7 maturation in the lysosome, and ultimately blocked the IMQ-induced NF-kappaB and IRF-7 nuclear translocation in DCs. Azithromycin 0-3 interferon regulatory factor 7 Mus musculus 146-151 27449383-10 2016 In addition to decreasing keratinocyte hyper-proliferation and restoring their terminal differentiation, AZM treatment decreased the accumulation of DCs as well as CD4, CD8 T cells and IL-17 producing cells in psoriatic skin lesions. Azithromycin 105-108 CD4 antigen Mus musculus 164-167 27449383-10 2016 In addition to decreasing keratinocyte hyper-proliferation and restoring their terminal differentiation, AZM treatment decreased the accumulation of DCs as well as CD4, CD8 T cells and IL-17 producing cells in psoriatic skin lesions. Azithromycin 105-108 interleukin 17A Mus musculus 185-190 27449383-11 2016 AZM treatment improved splenomegaly, decreased the populations of Th17 and gammadelta T cells, and reduced the expression of cytokines known to be involved in the pathogenesis of psoriasis, such as IL-17A, IL-17F, IL-22 and IL-23, in the skin and spleen. Azithromycin 0-3 interleukin 17F Mus musculus 206-212 27449383-11 2016 AZM treatment improved splenomegaly, decreased the populations of Th17 and gammadelta T cells, and reduced the expression of cytokines known to be involved in the pathogenesis of psoriasis, such as IL-17A, IL-17F, IL-22 and IL-23, in the skin and spleen. Azithromycin 0-3 interleukin 22 Mus musculus 214-219 27449383-11 2016 AZM treatment improved splenomegaly, decreased the populations of Th17 and gammadelta T cells, and reduced the expression of cytokines known to be involved in the pathogenesis of psoriasis, such as IL-17A, IL-17F, IL-22 and IL-23, in the skin and spleen. Azithromycin 0-3 interleukin 23, alpha subunit p19 Mus musculus 224-229 27449383-12 2016 CONCLUSION: AZM impaired IMQ-induced DC activation by decreasing lysosomal acidification and disrupting TLR7 maturation and signaling. Azithromycin 12-15 toll-like receptor 7 Mus musculus 104-108 27655795-5 2016 MMP-9 levels were measured using ELISA AZM enhanced barrier integrity (TEER/FITC-dextran), increased thickness, suppressed mucin production, and MMP-9 release during the formation of a normal epithelial barrier in vitro. Azithromycin 39-42 matrix metallopeptidase 9 Homo sapiens 0-5 27655795-6 2016 MMP-9 levels inversely correlated with TEER AZM also enhanced maintenance of the barrier and facilitated repair post-LPS challenge. Azithromycin 44-47 matrix metallopeptidase 9 Homo sapiens 0-5 27655795-11 2016 AZM also suppressed MMP-9 release which correlated with barrier integrity, suggesting a putative mechanism. Azithromycin 0-3 matrix metallopeptidase 9 Homo sapiens 20-25 27246785-8 2016 In contrast, IL-13-induced expression of POSTN was further increased in cells treated with azithromycin. Azithromycin 91-103 periostin Homo sapiens 41-46 27246785-0 2016 Azithromycin differentially affects the IL-13-induced expression profile in human bronchial epithelial cells. Azithromycin 0-12 interleukin 13 Homo sapiens 40-45 27246785-9 2016 This indicates that azithromycin has a differential effect on the IL-13-induced Th2 gene signature. Azithromycin 20-32 interleukin 13 Homo sapiens 66-71 27246785-3 2016 Clinical studies have shown that the macrolide antibiotic azithromycin reduced clinical symptoms in neutrophilic asthma, but not in the classical Th2-mediated asthma despite the ability of azithromycin to reduce IL-13-induced mucus production. Azithromycin 189-201 interleukin 13 Homo sapiens 212-217 27246785-4 2016 We therefore hypothesize that azithromycin differentially affects the IL-13-induced expression profile. Azithromycin 30-42 interleukin 13 Homo sapiens 70-75 27246785-10 2016 Furthermore, the ability of azithromycin to decrease IL-13-induced MUC5AC expression may be mediated by a reduction in CLCA1. Azithromycin 28-40 interleukin 13 Homo sapiens 53-58 27246785-7 2016 Azithromycin inhibited IL-13-induced MUC5AC, which was accompanied by inhibition of IL-13-induced CLCA1 and SERPINB2 expression. Azithromycin 0-12 interleukin 13 Homo sapiens 23-28 27246785-10 2016 Furthermore, the ability of azithromycin to decrease IL-13-induced MUC5AC expression may be mediated by a reduction in CLCA1. Azithromycin 28-40 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 67-73 27246785-7 2016 Azithromycin inhibited IL-13-induced MUC5AC, which was accompanied by inhibition of IL-13-induced CLCA1 and SERPINB2 expression. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 37-43 27246785-7 2016 Azithromycin inhibited IL-13-induced MUC5AC, which was accompanied by inhibition of IL-13-induced CLCA1 and SERPINB2 expression. Azithromycin 0-12 interleukin 13 Homo sapiens 84-89 27246785-10 2016 Furthermore, the ability of azithromycin to decrease IL-13-induced MUC5AC expression may be mediated by a reduction in CLCA1. Azithromycin 28-40 chloride channel accessory 1 Homo sapiens 119-124 27246785-7 2016 Azithromycin inhibited IL-13-induced MUC5AC, which was accompanied by inhibition of IL-13-induced CLCA1 and SERPINB2 expression. Azithromycin 0-12 chloride channel accessory 1 Homo sapiens 98-103 27392039-6 2016 injection of azithromycin (150 mg/kg) upon reperfusion prevented ischemia-induced spleen contraction and increased the number of MAC-1-immunopositive microglia/macrophages in the ischemic hemisphere 48 h after the insult. Azithromycin 13-25 integrin alpha M Mus musculus 129-134 27246785-7 2016 Azithromycin inhibited IL-13-induced MUC5AC, which was accompanied by inhibition of IL-13-induced CLCA1 and SERPINB2 expression. Azithromycin 0-12 serpin family B member 2 Homo sapiens 108-116 27246785-8 2016 In contrast, IL-13-induced expression of POSTN was further increased in cells treated with azithromycin. Azithromycin 91-103 interleukin 13 Homo sapiens 13-18 27156189-13 2016 Azithromycin reduced faecal biomarkers of environmental enteropathy (calprotectin, myeloperoxidase, alpha1-antitrypsin) and the prevalence of bacterial but not viral or eukaryotic pathogens. Azithromycin 0-12 myeloperoxidase Homo sapiens 83-98 27156189-13 2016 Azithromycin reduced faecal biomarkers of environmental enteropathy (calprotectin, myeloperoxidase, alpha1-antitrypsin) and the prevalence of bacterial but not viral or eukaryotic pathogens. Azithromycin 0-12 serpin family A member 1 Homo sapiens 100-118 27414503-13 2016 Reduced azithromycin susceptibility (Azi-RS) (defined as minimum inhibitory concentration [MIC] >=2.0 microg/mL) increased from 0.6% in 2013 to 2.5% in 2014. Azithromycin 8-20 antizyme inhibitor 1 Homo sapiens 37-40 26205530-5 2016 Our results showed that the expression of heat shock protein 70, proliferating cell nuclear antigen, vascular endothelial growth factor, caspase 3, and cytochrome P450 2E1 were significantly differently expressed during liver injury induced by 800 mg/kg AZ in mice. Azithromycin 254-256 caspase 3 Mus musculus 137-146 27350308-6 2016 Azithromycin transiently increased expression of IFNbeta and IFNlambda1 and RIG-I like helicases in un-infected COPD cells. Azithromycin 0-12 interferon beta 1 Homo sapiens 49-71 27350308-6 2016 Azithromycin transiently increased expression of IFNbeta and IFNlambda1 and RIG-I like helicases in un-infected COPD cells. Azithromycin 0-12 DExD/H-box helicase 58 Homo sapiens 76-81 27350308-7 2016 Further, azithromycin augmented RV16-induced expression of interferons and RIG-I like helicases in COPD cells but not in healthy epithelial cells. Azithromycin 9-21 DExD/H-box helicase 58 Homo sapiens 75-80 27350308-11 2016 Possibly by inducing expression of RIG-I like helicases, azithromycin increased rhinovirus-induced expression of interferons in COPD but not in healthy bronchial epithelium. Azithromycin 57-69 DExD/H-box helicase 58 Homo sapiens 35-40 26876435-4 2016 Here, we utilize the fat-1 transgenic mouse model, which can endogenously produce omega-3 fatty acids and thereby eliminates confounding factors of diet, to show that elevated tissue levels of omega-3 fatty acids significantly reduce body weight gain and the severity of insulin resistance, fatty liver and dyslipidemia resulting from early-life exposure to azithromycin. Azithromycin 358-370 FAT atypical cadherin 1 Mus musculus 21-26 27150818-0 2016 High azithromycin concentration in lungs by way of bovine serum albumin microspheres as targeted drug delivery: lung targeting efficiency in albino mice. Azithromycin 5-17 albumin Mus musculus 58-71 26876427-8 2016 Co-administration of IAP with AZT completely prevented this susceptibility by decreasing total body weight, serum lipids, glucose levels and liver lipids to the levels of control mice. Azithromycin 30-33 alkaline phosphatase 3, intestine, not Mn requiring Mus musculus 21-24 26876427-10 2016 CONCLUSIONS: Co-administration of IAP with AZT early in life prevents mice from susceptibility to the later development of MetS. Azithromycin 43-46 alkaline phosphatase 3, intestine, not Mn requiring Mus musculus 34-37 26205530-5 2016 Our results showed that the expression of heat shock protein 70, proliferating cell nuclear antigen, vascular endothelial growth factor, caspase 3, and cytochrome P450 2E1 were significantly differently expressed during liver injury induced by 800 mg/kg AZ in mice. Azithromycin 254-256 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 152-171 26751994-10 2016 CONCLUSIONS: Topically applied AZM can decrease TNF-alpha-induced apoptosis in corneal alkali burn. Azithromycin 31-34 tumor necrosis factor Rattus norvegicus 48-57 26832758-7 2016 Colistin and LL-37 strongly potentiated azithromycin killing of SM by increasing drug entry. Azithromycin 40-52 cathelicidin antimicrobial peptide Homo sapiens 13-18 26655749-0 2016 Azithromycin recovers reductions in barrier function in human gingival epithelial cells stimulated with tumor necrosis factor-alpha. Azithromycin 0-12 tumor necrosis factor Homo sapiens 104-131 26717512-5 2016 Two drugs with mechanisms of action novel to the COPD therapeutic arena (azithromycin and roflumilast) have been shown to reduce acute exacerbations of COPD. Azithromycin 73-85 COPD Homo sapiens 49-53 26717512-5 2016 Two drugs with mechanisms of action novel to the COPD therapeutic arena (azithromycin and roflumilast) have been shown to reduce acute exacerbations of COPD. Azithromycin 73-85 COPD Homo sapiens 152-156 26655749-5 2016 MATERIALS AND METHODS: HGEC were stimulated by tumor necrosis factor-alpha (TNF-alpha) in the presence of AZM or p38 MAP kinase and ERK inhibitors. Azithromycin 106-109 tumor necrosis factor Homo sapiens 47-74 26655749-5 2016 MATERIALS AND METHODS: HGEC were stimulated by tumor necrosis factor-alpha (TNF-alpha) in the presence of AZM or p38 MAP kinase and ERK inhibitors. Azithromycin 106-109 tumor necrosis factor Homo sapiens 76-85 26655749-9 2016 AZM inhibited the phosphorylation of ERK and p38 MAP kinase in TNF-alpha-stimulated HGEC. Azithromycin 0-3 mitogen-activated protein kinase 1 Homo sapiens 37-40 26655749-9 2016 AZM inhibited the phosphorylation of ERK and p38 MAP kinase in TNF-alpha-stimulated HGEC. Azithromycin 0-3 mitogen-activated protein kinase 14 Homo sapiens 45-59 26655749-9 2016 AZM inhibited the phosphorylation of ERK and p38 MAP kinase in TNF-alpha-stimulated HGEC. Azithromycin 0-3 tumor necrosis factor Homo sapiens 63-72 26655749-10 2016 Furthermore, AZM recovered the decrease in E-cadherin expression in HGEC stimulated with TNF-alpha. Azithromycin 13-16 cadherin 1 Homo sapiens 43-53 26655749-10 2016 Furthermore, AZM recovered the decrease in E-cadherin expression in HGEC stimulated with TNF-alpha. Azithromycin 13-16 tumor necrosis factor Homo sapiens 89-98 26655749-11 2016 CONCLUSIONS: These results suggested that AZM regulated gingival epithelial permeability through p38 MAP kinase and ERK signaling, and may contribute to suppress the inflammation in gingival tissue. Azithromycin 42-45 mitogen-activated protein kinase 14 Homo sapiens 97-100 26655749-11 2016 CONCLUSIONS: These results suggested that AZM regulated gingival epithelial permeability through p38 MAP kinase and ERK signaling, and may contribute to suppress the inflammation in gingival tissue. Azithromycin 42-45 mitogen-activated protein kinase 1 Homo sapiens 116-119 26430943-9 2015 RESULTS: In 300 samples, the susceptibility rates of GAS to penicillin, erythromycin, azithromycin, clindamycin, and tetracycline in northern Israel still remain very high. Azithromycin 86-98 gastrin Homo sapiens 53-56 26778828-9 2016 The concentrations of IL-5 and IL-13 in the OVA/LPS group decreased significantly after azithromycin administration. Azithromycin 88-100 interleukin 5 Mus musculus 22-26 26778828-9 2016 The concentrations of IL-5 and IL-13 in the OVA/LPS group decreased significantly after azithromycin administration. Azithromycin 88-100 interleukin 13 Mus musculus 31-36 26778828-10 2016 The levels of neutrophil elastase and IL-8, as surrogate markers of neutrophil activation, were reduced in the azithromycin group compared with the OVA/LPS group. Azithromycin 111-123 elastase, neutrophil expressed Mus musculus 14-33 26778828-10 2016 The levels of neutrophil elastase and IL-8, as surrogate markers of neutrophil activation, were reduced in the azithromycin group compared with the OVA/LPS group. Azithromycin 111-123 chemokine (C-X-C motif) ligand 15 Mus musculus 38-42 26778828-12 2016 The expression of MAPK/NF-kappaB signal and the level of BRP-39 in the lung decreased remarkably in the OVA/LPS with azithromycin-treated group. Azithromycin 117-129 chitinase-like 1 Mus musculus 57-63 26778828-13 2016 CONCLUSIONS: This study suggests that in a murine model of chronic asthma, long-term azithromycin treatment ameliorates not only airway inflammation but also airway remodeling by influencing on neutrophilc-related mediators, BRP-39 and MAPK/NF-kappaB signal pathways. Azithromycin 85-97 chitinase-like 1 Mus musculus 225-231 26228509-6 2015 KEY RESULTS: The expression levels of 3beta-HSD, CYP21, 11beta-HSD1 and CYP11B1 increased in human epithelial cells treated with clarithromycin and azithromycin, whereas the expression levels of 11beta-HSD2 and CYP11A1 were not affected. Azithromycin 148-160 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 38-47 26228509-6 2015 KEY RESULTS: The expression levels of 3beta-HSD, CYP21, 11beta-HSD1 and CYP11B1 increased in human epithelial cells treated with clarithromycin and azithromycin, whereas the expression levels of 11beta-HSD2 and CYP11A1 were not affected. Azithromycin 148-160 cytochrome P450 family 21 subfamily A member 2 Homo sapiens 49-54 26228509-6 2015 KEY RESULTS: The expression levels of 3beta-HSD, CYP21, 11beta-HSD1 and CYP11B1 increased in human epithelial cells treated with clarithromycin and azithromycin, whereas the expression levels of 11beta-HSD2 and CYP11A1 were not affected. Azithromycin 148-160 hydroxysteroid 11-beta dehydrogenase 1 Homo sapiens 56-67 26228509-6 2015 KEY RESULTS: The expression levels of 3beta-HSD, CYP21, 11beta-HSD1 and CYP11B1 increased in human epithelial cells treated with clarithromycin and azithromycin, whereas the expression levels of 11beta-HSD2 and CYP11A1 were not affected. Azithromycin 148-160 cytochrome P450 family 11 subfamily B member 1 Homo sapiens 72-79 26228509-9 2015 The expression of 3beta-HSD, CYP11A1, CYP21, CYP11B1 and 11beta-HSD1 was upregulated in nasal mucosa of mice treated with clarithromycin or azithromycin, but not in adrenalectomized mice. Azithromycin 140-152 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 18-27 26228509-9 2015 The expression of 3beta-HSD, CYP11A1, CYP21, CYP11B1 and 11beta-HSD1 was upregulated in nasal mucosa of mice treated with clarithromycin or azithromycin, but not in adrenalectomized mice. Azithromycin 140-152 cytochrome P450, family 11, subfamily a, polypeptide 1 Mus musculus 29-36 26228509-9 2015 The expression of 3beta-HSD, CYP11A1, CYP21, CYP11B1 and 11beta-HSD1 was upregulated in nasal mucosa of mice treated with clarithromycin or azithromycin, but not in adrenalectomized mice. Azithromycin 140-152 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 38-43 26228509-9 2015 The expression of 3beta-HSD, CYP11A1, CYP21, CYP11B1 and 11beta-HSD1 was upregulated in nasal mucosa of mice treated with clarithromycin or azithromycin, but not in adrenalectomized mice. Azithromycin 140-152 cytochrome P450, family 11, subfamily b, polypeptide 1 Mus musculus 45-52 26228509-9 2015 The expression of 3beta-HSD, CYP11A1, CYP21, CYP11B1 and 11beta-HSD1 was upregulated in nasal mucosa of mice treated with clarithromycin or azithromycin, but not in adrenalectomized mice. Azithromycin 140-152 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 57-68 26252749-8 2015 At specific times during healing, the azithromycin group exhibited significantly lower levels of interleukin (IL)-6 and IL-8 in GCF than the amoxicillin group and exhibited significantly lower levels of granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-gamma-inducible protein-10 in PICF. Azithromycin 38-50 C-X-C motif chemokine ligand 8 Homo sapiens 120-124 26252749-8 2015 At specific times during healing, the azithromycin group exhibited significantly lower levels of interleukin (IL)-6 and IL-8 in GCF than the amoxicillin group and exhibited significantly lower levels of granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-gamma-inducible protein-10 in PICF. Azithromycin 38-50 C-X-C motif chemokine ligand 8 Homo sapiens 242-246 26252749-8 2015 At specific times during healing, the azithromycin group exhibited significantly lower levels of interleukin (IL)-6 and IL-8 in GCF than the amoxicillin group and exhibited significantly lower levels of granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-gamma-inducible protein-10 in PICF. Azithromycin 38-50 C-C motif chemokine ligand 4 like 1 Homo sapiens 248-285 26252749-8 2015 At specific times during healing, the azithromycin group exhibited significantly lower levels of interleukin (IL)-6 and IL-8 in GCF than the amoxicillin group and exhibited significantly lower levels of granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-gamma-inducible protein-10 in PICF. Azithromycin 38-50 C-X-C motif chemokine ligand 10 Homo sapiens 291-328 26546328-1 2016 This study was performed in children with adenotonsillar hypertrophy to evaluate the effect of azithromycin (AZT) on the presence of NTHi in monocyte/macrophages (CD14(+) cells) of adenoids/tonsils and the persistence of NTHi after adenotonsillectomy. Azithromycin 95-107 CD14 molecule Homo sapiens 163-167 26546328-8 2016 AZT treatment followed by adenotonsillectomy did not completely eliminate NTHi from pharynges; however, it significantly reduced the risk of carriage of Haemophilus influenzae inside the CD14(+) cells. Azithromycin 0-3 CD14 molecule Homo sapiens 187-191 26820753-5 2016 Compared with non-molecularly imprinted polymer (NIP) electrodes, NIP/ABP electrodes, and MIP-modified carbon paste electrodes, MIP/ABP electrode exhibited excellent current response toward AZM. Azithromycin 190-193 amine oxidase copper containing 1 Homo sapiens 132-135 26291963-0 2015 The role of azithromycin in healthcare-associated pneumonia treatment. Azithromycin 12-24 structural maintenance of chromosomes 3 Homo sapiens 28-59 26291963-3 2015 Azithromycin is oftentimes included in the empiric treatment regimen for HCAP because of the importance of appropriate empiric antimicrobial coverage, the perceived concern regarding atypical organisms, potential anti-inflammatory effects of the medication, and positive clinical data among patients with Streptococcal bacteremia. Azithromycin 0-12 structural maintenance of chromosomes 3 Homo sapiens 73-77 26291963-4 2015 METHODS: In this review, we systematically investigate data for each of these topics along with clinical data examining the role of azithromycin in HCAP. Azithromycin 132-144 structural maintenance of chromosomes 3 Homo sapiens 148-152 25976224-8 2015 (1) Azithromycin reduced hERG currents by accelerated channel inactivation. Azithromycin 4-16 ETS transcription factor ERG Homo sapiens 25-29 26204109-1 2015 IMPORTANCE: Topical application of azithromycin suppresses expression of proinflammatory mediators while restoring transforming growth factor beta1 (TGF-beta1) levels as evaluated by eyelid margin and conjunctival impression cytology. Azithromycin 35-47 transforming growth factor beta 1 Homo sapiens 115-147 26204109-1 2015 IMPORTANCE: Topical application of azithromycin suppresses expression of proinflammatory mediators while restoring transforming growth factor beta1 (TGF-beta1) levels as evaluated by eyelid margin and conjunctival impression cytology. Azithromycin 35-47 transforming growth factor beta 1 Homo sapiens 149-158 26168736-3 2015 Some patients, while receiving azithromycin, (re)develop increased airway neutrophilia, which we hypothesize to result in worse outcome and to be regulated by an IL-17-independent mechanism. Azithromycin 31-43 interleukin 17A Homo sapiens 162-167 26204109-14 2015 CONCLUSIONS AND RELEVANCE: While the study did not control for potential confounding factors over time independent of the intervention that may have contributed to the results, topical azithromycin suppressed expression of proinflammatory mediators and increased expression of TGF-beta1 to normal levels. Azithromycin 185-197 transforming growth factor beta 1 Homo sapiens 277-286 26204109-15 2015 Increased TGF-beta1 expression may contribute to the anti-inflammatory activity of azithromycin in MGD. Azithromycin 83-95 transforming growth factor beta 1 Homo sapiens 10-19 25976224-9 2015 (2) The combination of Berberine with Azithromycin reduced hERG currents, producing an inhibitive effect stronger than use of a single drug alone, due to the high binding affinity for the onset of inactivation. Azithromycin 38-50 ETS transcription factor ERG Homo sapiens 59-63 26152605-6 2015 Azithromycin, but not clarithromycin or roxithromycin, specifically inhibited IL-1alpha and IL-1beta secretion upon LPS stimulation. Azithromycin 0-12 interleukin 1 alpha Mus musculus 78-87 26152605-10 2015 Furthermore, azithromycin specifically affected IL-1beta levels in a murine endotoxin sepsis model. Azithromycin 13-25 interleukin 1 beta Mus musculus 48-56 26152605-6 2015 Azithromycin, but not clarithromycin or roxithromycin, specifically inhibited IL-1alpha and IL-1beta secretion upon LPS stimulation. Azithromycin 0-12 interleukin 1 beta Mus musculus 92-100 25458910-0 2015 Randomized trial to evaluate azithromycin"s effects on serum and upper airway IL-8 levels and recurrent wheezing in infants with respiratory syncytial virus bronchiolitis. Azithromycin 29-41 C-X-C motif chemokine ligand 8 Homo sapiens 78-82 25407884-5 2015 Azithromycin produced almost complete inhibition of both cytokines, but tended to be less potent than rolipram (IC50 10.66 and 17.4 mum for TNF-alpha and IL-1beta, respectively). Azithromycin 0-12 interleukin-1 beta Equus caballus 154-162 25791017-0 2015 Effect of azithromycin on the LPS-induced production and secretion of phospholipase A2 in lung cells. Azithromycin 10-22 phospholipase A2 group IB Homo sapiens 70-86 25791017-4 2015 The aim of the study was to investigate whether in lung cells azithromycin can inhibit secretory and cytosolic phospholipases A2, (sPLA2) and (cPLA2), respectively, which are induced by an inflammatory trigger. Azithromycin 62-74 phospholipase A2 group IIA Homo sapiens 131-136 25791017-4 2015 The aim of the study was to investigate whether in lung cells azithromycin can inhibit secretory and cytosolic phospholipases A2, (sPLA2) and (cPLA2), respectively, which are induced by an inflammatory trigger. Azithromycin 62-74 phospholipase A2 group IVA Homo sapiens 143-148 25791017-6 2015 Pre-treatment of cells with azithromycin caused a dose-dependent decrease in the LPS-induced sPLA2-IIA levels in A549 cells. Azithromycin 28-40 phospholipase A2 group IIA Homo sapiens 93-98 25791017-10 2015 We conclude that azithromycin exerts anti-inflammatory properties on lung epithelial cells through the inhibition of both the expression and secretion of LPS-induced sPLA2-IIA, while it does not affect alveolar macrophages. Azithromycin 17-29 phospholipase A2 group IIA Homo sapiens 166-171 25058850-4 2015 AZM significantly upregulated NLRC1 and NLRC2 while NAC upregulated only NLRC2 receptor expression in CF cells. Azithromycin 0-3 nucleotide binding oligomerization domain containing 1 Homo sapiens 30-35 25058850-4 2015 AZM significantly upregulated NLRC1 and NLRC2 while NAC upregulated only NLRC2 receptor expression in CF cells. Azithromycin 0-3 nucleotide binding oligomerization domain containing 2 Homo sapiens 40-45 25058850-6 2015 MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2. Azithromycin 32-35 interleukin 6 Homo sapiens 83-87 25058850-6 2015 MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2. Azithromycin 32-35 interleukin 6 Homo sapiens 140-144 25458910-3 2015 OBJECTIVES: We sought to investigate whether azithromycin treatment during RSV bronchiolitis reduces serum and nasal lavage IL-8 levels and the occurrence of postbronchiolitis recurrent wheezing. Azithromycin 45-57 C-X-C motif chemokine ligand 8 Homo sapiens 124-128 25607112-10 2015 AZM significantly attenuated the CSE-induced decreases in the expression of VEGF and epithelial cell structural proteins, including ZO-1 and occludin. Azithromycin 0-3 vascular endothelial growth factor A Homo sapiens 76-80 25607112-10 2015 AZM significantly attenuated the CSE-induced decreases in the expression of VEGF and epithelial cell structural proteins, including ZO-1 and occludin. Azithromycin 0-3 tight junction protein 1 Homo sapiens 132-136 25607112-10 2015 AZM significantly attenuated the CSE-induced decreases in the expression of VEGF and epithelial cell structural proteins, including ZO-1 and occludin. Azithromycin 0-3 occludin Homo sapiens 141-149 25607112-12 2015 In addition, the inhibition of ROS by N-acetyl-L-cysteine had similar effects as AZM on the expression of VEGF and epithelial cell structural proteins and also enhanced cell proliferation. Azithromycin 81-84 vascular endothelial growth factor A Homo sapiens 106-110 25458910-7 2015 RESULTS: Compared with placebo, azithromycin treatment did not reduce serum IL-8 levels at day 8 (P = .6) but resulted in a greater decrease in nasal lavage fluid IL-8 levels by day 15 (P = .03). Azithromycin 32-44 C-X-C motif chemokine ligand 8 Homo sapiens 163-167 25458910-10 2015 CONCLUSION: In this proof-of-concept study azithromycin treatment during RSV bronchiolitis reduced upper airway IL-8 levels, prolonged the time to the third wheezing episode, and reduced overall respiratory morbidity over the subsequent year. Azithromycin 43-55 C-X-C motif chemokine ligand 8 Homo sapiens 112-116 27128001-6 2015 Alisporivir as an inhibitor of CYP3A4 caused a 39% increase in azithromycin exposure. Azithromycin 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25595376-10 2015 Azithromycin reduced interleukin-17 expression (P = .049) and the number of IL-17(+)/CD8(+) lymphocytes at 4 weeks, and active matrix metalloprotease-9 at 8 weeks (P = .017), and increased interleukin-12 expression (P = .025) at 8 weeks following transplantation versus control allografts. Azithromycin 0-12 interleukin 17A Rattus norvegicus 76-81 24806810-2 2015 This study aimed to investigate the effect of azithromycin on the production of pro-inflammatory cytokines and chemokines by human gingival fibroblasts (HGF) in vitro. Azithromycin 46-58 hepatocyte growth factor Homo sapiens 153-156 24806810-5 2015 RESULTS: P. gingivalis LPS induced cytokine/chemokine (IL-6, IL-8, MCP-1, and GRO) protein production in HGFs, and this effect was suppressed by azithromycin at all concentrations tested. Azithromycin 145-157 interleukin 6 Homo sapiens 55-59 24806810-5 2015 RESULTS: P. gingivalis LPS induced cytokine/chemokine (IL-6, IL-8, MCP-1, and GRO) protein production in HGFs, and this effect was suppressed by azithromycin at all concentrations tested. Azithromycin 145-157 C-X-C motif chemokine ligand 8 Homo sapiens 61-65 24806810-5 2015 RESULTS: P. gingivalis LPS induced cytokine/chemokine (IL-6, IL-8, MCP-1, and GRO) protein production in HGFs, and this effect was suppressed by azithromycin at all concentrations tested. Azithromycin 145-157 C-C motif chemokine ligand 2 Homo sapiens 67-72 24806810-6 2015 CONCLUSIONS: This study demonstrates that azithromycin suppresses P. gingivalis LPS-induced cytokine/chemokine protein production in HGF, which may explain some of the clinical benefits observed with the adjunctive use of azithromycin in the treatment of periodontitis. Azithromycin 42-54 hepatocyte growth factor Homo sapiens 133-136 24806810-6 2015 CONCLUSIONS: This study demonstrates that azithromycin suppresses P. gingivalis LPS-induced cytokine/chemokine protein production in HGF, which may explain some of the clinical benefits observed with the adjunctive use of azithromycin in the treatment of periodontitis. Azithromycin 222-234 hepatocyte growth factor Homo sapiens 133-136 25359346-12 2015 Furthermore, azithromycin increased RV-induced pattern recognition receptor, IFN and IFN-stimulated gene mRNA levels. Azithromycin 13-25 interferon alpha 1 Homo sapiens 77-80 25359346-12 2015 Furthermore, azithromycin increased RV-induced pattern recognition receptor, IFN and IFN-stimulated gene mRNA levels. Azithromycin 13-25 interferon alpha 1 Homo sapiens 85-88 25359346-14 2015 Azithromycin pre-treatment reduces RV replication in CF bronchial epithelial cells, possibly through the amplification of the antiviral response mediated by the IFN pathway. Azithromycin 0-12 interferon alpha 1 Homo sapiens 161-164 25604277-9 2015 Oral therapy with AZM (500 mg/kg) and CIP (30 mg/kg) combination in mice for 4 days showed accelerated clearance of bacteria from kidney and bladder tissue, improved renal histopathology, decreased levels of MDA and NO, significant decline in MIP-2 and IL-6, and increased IL-10 in the kidney (P<0.0001). Azithromycin 18-21 chemokine (C-X-C motif) ligand 2 Mus musculus 243-248 25604277-9 2015 Oral therapy with AZM (500 mg/kg) and CIP (30 mg/kg) combination in mice for 4 days showed accelerated clearance of bacteria from kidney and bladder tissue, improved renal histopathology, decreased levels of MDA and NO, significant decline in MIP-2 and IL-6, and increased IL-10 in the kidney (P<0.0001). Azithromycin 18-21 interleukin 6 Mus musculus 253-257 25604277-9 2015 Oral therapy with AZM (500 mg/kg) and CIP (30 mg/kg) combination in mice for 4 days showed accelerated clearance of bacteria from kidney and bladder tissue, improved renal histopathology, decreased levels of MDA and NO, significant decline in MIP-2 and IL-6, and increased IL-10 in the kidney (P<0.0001). Azithromycin 18-21 interleukin 10 Mus musculus 273-278 25747269-13 2015 The costs of azithromycin PEP among infants, children and adults were $1,976, $132 and $90, respectively. Azithromycin 13-25 prolyl endopeptidase Homo sapiens 26-29 25611398-9 2015 These differentiative actions of azithromycin were paralleled by an increased expression of sterol regulatory element-binding protein 1. Azithromycin 33-45 sterol regulatory element binding transcription factor 1 Homo sapiens 92-135 25534598-9 2015 INTERPRETATION: Among older adults taking a statin not metabolized by CYP3A4, co-prescription of clarithromycin versus azithromycin was associated with a modest but statistically significant increase in the 30-day absolute risk of adverse outcomes. Azithromycin 119-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 25445642-8 2015 In vitro, allogeneic antigen-presenting cell (APC)- dependent T cell proliferation and cytokine production were suppressed by azithromycin and inversely correlated with relative regulatory T cell (Treg) expansion, whereas no effect was seen when T cell proliferation occurred APC independently through CD3/CD28-stimulation. Azithromycin 126-138 CD3 antigen, epsilon polypeptide Mus musculus 302-305 25445642-8 2015 In vitro, allogeneic antigen-presenting cell (APC)- dependent T cell proliferation and cytokine production were suppressed by azithromycin and inversely correlated with relative regulatory T cell (Treg) expansion, whereas no effect was seen when T cell proliferation occurred APC independently through CD3/CD28-stimulation. Azithromycin 126-138 CD28 antigen Mus musculus 306-310 25445642-9 2015 Further, azithromycin reduced alloreactive T cell expansion but increased Treg expansion in vivo with corresponding downregulation of MHC II on CD11c(+) dendritic cells. Azithromycin 9-21 integrin subunit alpha X Homo sapiens 144-149 27025048-8 2015 Azithromycin-induced increase in water absorption was associated with upregulation of AQP 8 water channel expression (P < 0.05) in colonic mucosa. Azithromycin 0-12 aquaporin 8 Rattus norvegicus 86-91 25308201-0 2015 Increased CD8 T-cell granzyme B in COPD is suppressed by treatment with low-dose azithromycin. Azithromycin 81-93 CD8a molecule Homo sapiens 10-13 25249648-10 2015 As confirmed by western blotting, the levels of VEGF in lung homogenates were higher in the Azm-treated group than in the COPD, saline-treated, and Lev-treated groups. Azithromycin 92-95 vascular endothelial growth factor A Rattus norvegicus 48-52 25249648-11 2015 VEGFR2 protein expression was higher in the Azm-treated group than in the COPD, saline-treated, and Lev-treated groups. Azithromycin 44-47 kinase insert domain receptor Rattus norvegicus 0-6 25249648-12 2015 CONCLUSIONS: Azm attenuates pulmonary emphysema by partly reversing the decrease in the numbers of inflammatory cells (neutrophil and macrophage) and VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats. Azithromycin 13-16 vascular endothelial growth factor A Rattus norvegicus 150-154 25249648-12 2015 CONCLUSIONS: Azm attenuates pulmonary emphysema by partly reversing the decrease in the numbers of inflammatory cells (neutrophil and macrophage) and VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats. Azithromycin 13-16 kinase insert domain receptor Rattus norvegicus 169-175 25308201-0 2015 Increased CD8 T-cell granzyme B in COPD is suppressed by treatment with low-dose azithromycin. Azithromycin 81-93 granzyme B Homo sapiens 21-31 25308201-5 2015 We previously showed that low-dose azithromycin reduced airways inflammation in COPD subjects and we hypothesized that it would also reduce granzyme B production by CD8 T cells. Azithromycin 35-47 granzyme B Homo sapiens 140-150 25308201-5 2015 We previously showed that low-dose azithromycin reduced airways inflammation in COPD subjects and we hypothesized that it would also reduce granzyme B production by CD8 T cells. Azithromycin 35-47 CD8a molecule Homo sapiens 165-168 25308201-8 2015 RESULTS: T-cell granzyme B production in both airway and intra-epithelial compartments was reduced in COPD patients following 12 weeks of azithromycin treatment, with no significant effect in blood. Azithromycin 138-150 granzyme B Homo sapiens 16-26 25308201-9 2015 Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro. Azithromycin 5-17 CD4 molecule Homo sapiens 51-54 25308201-9 2015 Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro. Azithromycin 5-17 granzyme B Homo sapiens 62-72 25308201-9 2015 Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro. Azithromycin 94-106 CD8a molecule Homo sapiens 133-136 25308201-9 2015 Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro. Azithromycin 94-106 granzyme B Homo sapiens 145-155 25009233-7 2014 Induction of PPARgamma, shown to play a role in AAM development, by the PPARgamma agonist rosiglitazone or treatment of mice with the macrolide antibiotic AZM, also reported to skew macrophage differentiation to an AAM phenotype, increased the AAM markers and mitigated RSV-induced lung pathology. Azithromycin 155-158 peroxisome proliferator activated receptor gamma Mus musculus 13-22 25500904-0 2014 Azithromycin suppresses CD4(+) T-cell activation by direct modulation of mTOR activity. Azithromycin 0-12 CD4 molecule Homo sapiens 24-27 25500904-0 2014 Azithromycin suppresses CD4(+) T-cell activation by direct modulation of mTOR activity. Azithromycin 0-12 mechanistic target of rapamycin kinase Homo sapiens 73-77 25500904-6 2014 AZM inhibited cell proliferation rate and cytokine secretion of CD4(+) T-cells in a dose-dependent manner. Azithromycin 0-3 CD4 molecule Homo sapiens 64-67 25500904-8 2014 Analysis of molecular signaling pathways revealed that exposure to AZM reduced the phosphorylation of the S6 ribosomal protein, a downstream target of mTOR. Azithromycin 67-70 mechanistic target of rapamycin kinase Homo sapiens 151-155 25500904-10 2014 In vitro kinase studies using recombinant mTOR showed that AZM inhibited mTOR activity. Azithromycin 59-62 mechanistic target of rapamycin kinase Homo sapiens 42-46 25500904-10 2014 In vitro kinase studies using recombinant mTOR showed that AZM inhibited mTOR activity. Azithromycin 59-62 mechanistic target of rapamycin kinase Homo sapiens 73-77 25500904-12 2014 We show for the first time that AZM and to a lesser extent CLM act as immunosuppressive agents on CD4(+) T-cells by inhibiting mTOR activity. Azithromycin 32-35 CD4 molecule Homo sapiens 98-101 25500904-12 2014 We show for the first time that AZM and to a lesser extent CLM act as immunosuppressive agents on CD4(+) T-cells by inhibiting mTOR activity. Azithromycin 32-35 mechanistic target of rapamycin kinase Homo sapiens 127-131 25155592-8 2014 The model-predicted unionized azithromycin (AZM) concentrations in the cytosol of PMLs (6.0 +- 1.2 ng/ml) were comparable to the measured ISF concentrations in the muscle (8.7 +- 2.9 ng/ml) and subcutis (4.1 +- 2.4 ng/ml) on day 10, whereas the total PML concentrations were >1,000-fold higher (14,217 +- 2,810 ng/ml). Azithromycin 30-42 PML nuclear body scaffold Homo sapiens 82-85 25155592-8 2014 The model-predicted unionized azithromycin (AZM) concentrations in the cytosol of PMLs (6.0 +- 1.2 ng/ml) were comparable to the measured ISF concentrations in the muscle (8.7 +- 2.9 ng/ml) and subcutis (4.1 +- 2.4 ng/ml) on day 10, whereas the total PML concentrations were >1,000-fold higher (14,217 +- 2,810 ng/ml). Azithromycin 44-47 PML nuclear body scaffold Homo sapiens 82-85 24631273-5 2014 Initial, stimulatory effects of azithromycin on immune and epithelial cells, involving interactions with phospholipids and Erk1/2, are followed by later modulation of transcription factors AP-1, NFkappaB, inflammatory cytokine and mucin release. Azithromycin 32-44 mitogen-activated protein kinase 3 Homo sapiens 123-129 29114567-0 2014 Azithromycin and COPD Exacerbations in the Presence or Absence of Symptoms or Active Treatment for Gastroesophageal Reflux. Azithromycin 0-12 GER Homo sapiens 99-122 25148049-0 2014 The effect of azithromycin in adults with stable neutrophilic COPD: a double blind randomised, placebo controlled trial. Azithromycin 14-26 COPD Homo sapiens 62-66 25148049-4 2014 This study tested the hypothesis that azithromycin treatment, as an add-on to standard medication, would significantly reduce airway neutrophil and neutrophils chemokine (CXCL8) levels, as well as bacterial load. Azithromycin 38-50 C-X-C motif chemokine ligand 8 Homo sapiens 171-176 25148049-12 2014 Azithromycin treatment resulted in a non-significant reduction in sputum neutrophil proportion, CXCL8 levels and bacterial load. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 96-101 25148049-15 2014 CONCLUSIONS: In stable COPD with neutrophilic bronchitis, add-on azithromycin therapy showed a trend to reduced severe exacerbations sputum neutrophils, CXCL8 levels and bacterial load. Azithromycin 65-77 COPD Homo sapiens 23-27 25148049-15 2014 CONCLUSIONS: In stable COPD with neutrophilic bronchitis, add-on azithromycin therapy showed a trend to reduced severe exacerbations sputum neutrophils, CXCL8 levels and bacterial load. Azithromycin 65-77 C-X-C motif chemokine ligand 8 Homo sapiens 153-158 24890593-6 2014 Respiratory epithelial cell-derived MMP-3 was suppressed by moxifloxacin, rifampicin, and azithromycin in a dose-dependent manner. Azithromycin 90-102 matrix metallopeptidase 3 Homo sapiens 36-41 24890593-7 2014 Respiratory epithelial cell-derived MMP-1 was suppressed by moxifloxacin and azithromycin, whereas MMP-9 secretion was only decreased by moxifloxacin. Azithromycin 77-89 matrix metallopeptidase 1 Homo sapiens 36-41 24890593-8 2014 In contrast, moxifloxacin and azithromycin both increased MMP-1 and -3 secretion from MRC-5 fibroblasts, demonstrating that the effects of these drugs are cell specific. Azithromycin 30-42 matrix metallopeptidase 1 Homo sapiens 58-70 25505605-1 2014 We studied in vivo the potential involvement of nuclear factor-kappaB (NF-kappaB) pathway in the molecular mechanism of the anti-inflammatory and immunomodulatory activity of azithromycin in the lung. Azithromycin 175-187 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 71-80 25505605-6 2014 Pretreatment with azithromycin significantly decreased lung bioluminescence and airways cell infiltration induced by LPS, also reducing proinflammatory cytokines concentrations in bronchoalveolar lavages and inhibiting NF-kappaB nuclear translocation. Azithromycin 18-30 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 219-228 25505605-7 2014 The results obtained using a novel approach to monitor NF-kappaB activation, provided, for the first time, in vivo evidence that azithromycin treatment results in pulmonary anti-inflammatory activity associated with the inhibition of NF-kappaB activation in the lung. Azithromycin 129-141 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 55-64 25505605-7 2014 The results obtained using a novel approach to monitor NF-kappaB activation, provided, for the first time, in vivo evidence that azithromycin treatment results in pulmonary anti-inflammatory activity associated with the inhibition of NF-kappaB activation in the lung. Azithromycin 129-141 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 234-243 24631273-5 2014 Initial, stimulatory effects of azithromycin on immune and epithelial cells, involving interactions with phospholipids and Erk1/2, are followed by later modulation of transcription factors AP-1, NFkappaB, inflammatory cytokine and mucin release. Azithromycin 32-44 nuclear factor kappa B subunit 1 Homo sapiens 195-203 24716633-0 2014 Increased IL-8 production in human bronchial epithelial cells after exposure to azithromycin-pretreated Pseudomonas aeruginosa in vitro. Azithromycin 80-92 C-X-C motif chemokine ligand 8 Homo sapiens 10-14 24716633-4 2014 The results showed that AZM-pretreated P. aeruginosa (PAO1 and six different clinical isolates) significantly stimulated HBE cells to release IL-8, a crucial pro-inflammatory cytokine. Azithromycin 24-27 C-X-C motif chemokine ligand 8 Homo sapiens 142-146 24716633-6 2014 Our results suggest that AZM-pretreated P. aeruginosa could indirectly exacerbate pro-inflammation by inducing IL-8 production in HBEs. Azithromycin 25-28 C-X-C motif chemokine ligand 8 Homo sapiens 111-115 24378875-5 2014 RECENT FINDINGS: Two well designed, randomized, placebo-controlled trials report that select patients treated for 1 year with erythromycin or azithromycin, in addition to usual care, have prolonged time to and lower frequency of COPD exacerbations. Azithromycin 142-154 COPD Homo sapiens 229-233 26625370-2 2014 We found that exposure of pneumococci to AZM led to reduced tumor necrosis factor (TNF) secretion by macrophages; this effect was observed in response to both AZM-susceptible and AZM-resistant (AZM-R) pneumococci. Azithromycin 41-44 tumor necrosis factor Homo sapiens 60-81 26625370-2 2014 We found that exposure of pneumococci to AZM led to reduced tumor necrosis factor (TNF) secretion by macrophages; this effect was observed in response to both AZM-susceptible and AZM-resistant (AZM-R) pneumococci. Azithromycin 41-44 tumor necrosis factor Homo sapiens 83-86 24534490-3 2014 The present study was designed to investigate the effect of the macrolide antibiotic azithromycin on IL-6 generation in murine macrophages treated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action. Azithromycin 85-97 interleukin 6 Mus musculus 101-105 24534490-3 2014 The present study was designed to investigate the effect of the macrolide antibiotic azithromycin on IL-6 generation in murine macrophages treated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action. Azithromycin 85-97 toll-like receptor 4 Mus musculus 172-175 24534490-4 2014 Azithromycin significantly suppressed IL-6 production as well as its mRNA expression in P. intermedia LPS-activated RAW264.7 cells. Azithromycin 0-12 interleukin 6 Mus musculus 38-42 24534490-4 2014 Azithromycin significantly suppressed IL-6 production as well as its mRNA expression in P. intermedia LPS-activated RAW264.7 cells. Azithromycin 0-12 toll-like receptor 4 Mus musculus 102-105 24534490-7 2014 Instead, azithromycin significantly diminished nuclear translocation and DNA binding activity of NF-kappaB p50 subunit induced with LPS. Azithromycin 9-21 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 97-106 24534490-7 2014 Instead, azithromycin significantly diminished nuclear translocation and DNA binding activity of NF-kappaB p50 subunit induced with LPS. Azithromycin 9-21 toll-like receptor 4 Mus musculus 132-135 24534490-8 2014 Azithromycin inhibited P. intermedia LPS-induced STAT1 and STAT3 phosphorylation. Azithromycin 0-12 toll-like receptor 4 Mus musculus 37-40 24534490-8 2014 Azithromycin inhibited P. intermedia LPS-induced STAT1 and STAT3 phosphorylation. Azithromycin 0-12 signal transducer and activator of transcription 1 Mus musculus 49-54 24534490-8 2014 Azithromycin inhibited P. intermedia LPS-induced STAT1 and STAT3 phosphorylation. Azithromycin 0-12 signal transducer and activator of transcription 3 Mus musculus 59-64 24534490-9 2014 In addition, azithromycin up-regulated the mRNA level of SOCS1 in cells treated with LPS. Azithromycin 13-25 suppressor of cytokine signaling 1 Mus musculus 57-62 24534490-9 2014 In addition, azithromycin up-regulated the mRNA level of SOCS1 in cells treated with LPS. Azithromycin 13-25 toll-like receptor 4 Mus musculus 85-88 24417187-8 2014 However, only azithromycin reduced IL-1beta levels in the lung 24 h post LPS challenge. Azithromycin 14-26 interleukin 1 beta Mus musculus 35-43 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 toll-like receptor 4 Mus musculus 67-70 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 interleukin 6 Mus musculus 93-97 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 138-147 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 signal transducer and activator of transcription 1 Mus musculus 149-154 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 signal transducer and activator of transcription 3 Mus musculus 159-164 24534490-10 2014 In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-kappaB, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Azithromycin 15-27 suppressor of cytokine signaling 1 Mus musculus 224-229 23879671-11 2013 CONCLUSIONS: Azithromycin treatment decreased the mucocutaneous manifestations in BD patients and suppressed the intracellular IFN-gamma responses of PBMCs to S. sanguinis ex vivo, which suggests this treatment has an immunomodulatory effect. Azithromycin 13-25 interferon gamma Homo sapiens 127-136 24018177-5 2014 RESULTS: Expression of NOS2 and TNFalpha was decreased in subjects receiving azithromycin, whereas expression of M2-associated genes was unaffected. Azithromycin 77-89 nitric oxide synthase 2 Homo sapiens 23-27 24018177-5 2014 RESULTS: Expression of NOS2 and TNFalpha was decreased in subjects receiving azithromycin, whereas expression of M2-associated genes was unaffected. Azithromycin 77-89 tumor necrosis factor Homo sapiens 32-40 24556631-8 2014 RESULTS: AZM and MDM attenuated PMA-induced MUC5AC and MUC2 gene and protein expression in NCI-H292 cells. Azithromycin 9-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 44-50 24556631-8 2014 RESULTS: AZM and MDM attenuated PMA-induced MUC5AC and MUC2 gene and protein expression in NCI-H292 cells. Azithromycin 9-12 mucin 2, oligomeric mucus/gel-forming Homo sapiens 55-59 24556631-10 2014 CONCLUSION: The present study demonstrates that AZM and MDM suppress the synthesis of mucin and TNF-alpha from human airway epithelial cells. Azithromycin 48-51 LOC100508689 Homo sapiens 86-91 24556631-10 2014 CONCLUSION: The present study demonstrates that AZM and MDM suppress the synthesis of mucin and TNF-alpha from human airway epithelial cells. Azithromycin 48-51 tumor necrosis factor Homo sapiens 96-105 24426177-0 2014 Azithromycin Reduces the Production of alpha-hemolysin and Biofilm Formation in Staphylococcus aureus. Azithromycin 0-12 AT695_RS11870 Staphylococcus aureus 39-54 24426177-4 2014 Azithromycin at subinhibitory concentration, markedly reduced the production of alpha-hemolysin at (1/16MIC, 1/8MIC) and biofilm formation at (1/16MIC, 1/8MIC), respectively. Azithromycin 0-12 AT695_RS11870 Staphylococcus aureus 80-95 24426177-5 2014 The results indicated that sub-inhibitory concentrations of azithromycin decreased the production of alpha-hemolysin and biofilm formation in MRSA in a dose-dependent manner. Azithromycin 60-72 AT695_RS11870 Staphylococcus aureus 101-116 24426177-6 2014 Therefore, azithromycin may be useful in the treatment of alpha-hemolysin producing and biofilm formation MRSA infections. Azithromycin 11-23 AT695_RS11870 Staphylococcus aureus 58-73 24556631-3 2014 This study was designed to investigate the effect of azithromycin (AZM; 15-membered) and midecamycin acetate (MDM; 16-membered) on MUC5AC and MUC2 gene expression and secretion from human airway epithelial cells. Azithromycin 53-65 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 131-137 24556631-3 2014 This study was designed to investigate the effect of azithromycin (AZM; 15-membered) and midecamycin acetate (MDM; 16-membered) on MUC5AC and MUC2 gene expression and secretion from human airway epithelial cells. Azithromycin 53-65 mucin 2, oligomeric mucus/gel-forming Homo sapiens 142-146 24556631-3 2014 This study was designed to investigate the effect of azithromycin (AZM; 15-membered) and midecamycin acetate (MDM; 16-membered) on MUC5AC and MUC2 gene expression and secretion from human airway epithelial cells. Azithromycin 67-70 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 131-137 24556631-3 2014 This study was designed to investigate the effect of azithromycin (AZM; 15-membered) and midecamycin acetate (MDM; 16-membered) on MUC5AC and MUC2 gene expression and secretion from human airway epithelial cells. Azithromycin 67-70 mucin 2, oligomeric mucus/gel-forming Homo sapiens 142-146 24366582-6 2013 RESULTS: Azithromycin treatment significantly reduced sputum levels of PGP and myeloperoxidase in patients with COPD, particularly with increased duration of therapy. Azithromycin 9-21 myeloperoxidase Homo sapiens 79-94 24380240-0 2013 Azithromycin inhibits double-stranded RNA-induced thymic stromal lymphopoietin release from human airway epithelial cells. Azithromycin 0-12 thymic stromal lymphopoietin Homo sapiens 50-78 22205500-8 2013 Furthermore, azithromycin and dexamethasone significantly reduced both the VEGF release and the activation of p38(MAPK) pathway in response to FGF-1 or FGF-2 treatment. Azithromycin 13-25 vascular endothelial growth factor A Homo sapiens 75-79 22205500-8 2013 Furthermore, azithromycin and dexamethasone significantly reduced both the VEGF release and the activation of p38(MAPK) pathway in response to FGF-1 or FGF-2 treatment. Azithromycin 13-25 mitogen-activated protein kinase 1 Homo sapiens 110-113 22205500-8 2013 Furthermore, azithromycin and dexamethasone significantly reduced both the VEGF release and the activation of p38(MAPK) pathway in response to FGF-1 or FGF-2 treatment. Azithromycin 13-25 fibroblast growth factor 1 Homo sapiens 143-148 22205500-8 2013 Furthermore, azithromycin and dexamethasone significantly reduced both the VEGF release and the activation of p38(MAPK) pathway in response to FGF-1 or FGF-2 treatment. Azithromycin 13-25 fibroblast growth factor 2 Homo sapiens 152-157 22205500-10 2013 Both azithromycin and dexamethasone elicited their anti-angiogenic effects via p38(MAPK) pathway in vitro, thereby suggesting a possible therapeutic approach to tackle VEGF-mediated vascular remodeling. Azithromycin 5-17 mitogen-activated protein kinase 1 Homo sapiens 79-82 22205500-10 2013 Both azithromycin and dexamethasone elicited their anti-angiogenic effects via p38(MAPK) pathway in vitro, thereby suggesting a possible therapeutic approach to tackle VEGF-mediated vascular remodeling. Azithromycin 5-17 vascular endothelial growth factor A Homo sapiens 168-172 22205500-0 2013 Azithromycin attenuates fibroblast growth factors induced vascular endothelial growth factor via p38(MAPK) signaling in human airway smooth muscle cells. Azithromycin 0-12 vascular endothelial growth factor A Homo sapiens 58-92 22205500-0 2013 Azithromycin attenuates fibroblast growth factors induced vascular endothelial growth factor via p38(MAPK) signaling in human airway smooth muscle cells. Azithromycin 0-12 mitogen-activated protein kinase 1 Homo sapiens 97-100 24380240-4 2013 However, the effect of azithromycin on the production of TSLP has not been studied. Azithromycin 23-35 thymic stromal lymphopoietin Homo sapiens 57-61 24380240-5 2013 Here we explored the effects of azithromycin on viral surrogate (dsRNA)-induced TSLP in normal human bronchial epithelial (NHBE) cells. Azithromycin 32-44 thymic stromal lymphopoietin Homo sapiens 80-84 24380240-8 2013 We demonstrated that azithromycin inhibited the production and mRNA expression of TSLP in NHBE cells. Azithromycin 21-33 thymic stromal lymphopoietin Homo sapiens 82-86 24380240-9 2013 Azithromycin also inhibited the nuclear factor-KB luciferase activity induced by poly (I:C), and it prevented dsRNA-induced loss of the NF-kappaB repressor protein IkappaBalpha. Azithromycin 0-12 NFKB inhibitor alpha Homo sapiens 164-176 24380240-10 2013 These results suggest that azithromycin can be useful to treat asthma exacerbations due to the inhibition of TSLP. Azithromycin 27-39 thymic stromal lymphopoietin Homo sapiens 109-113 24292287-7 2013 A relatively higher rate of resistance to gentamicin, co-trimoxazole, azithromycin and quinolones were also observed for ESBL producers. Azithromycin 70-82 EsbL Escherichia coli 121-125 23527897-2 2013 Since macrolide antibiotics, such as clarithromycin and azithromycin, exert immunomodulatory effects, they would affect the Kv1.3-channel currents in lymphocytes. Azithromycin 56-68 potassium voltage-gated channel, shaker-related subfamily, member 3 Mus musculus 124-129 23199585-7 2013 CAM and AZM induced a dose-dependent suppression of spontaneous TNF-alpha, sTNFR2, IL-6, IL-8 and CCL18 production (p<0.05). Azithromycin 8-11 tumor necrosis factor Homo sapiens 64-73 23199585-7 2013 CAM and AZM induced a dose-dependent suppression of spontaneous TNF-alpha, sTNFR2, IL-6, IL-8 and CCL18 production (p<0.05). Azithromycin 8-11 interleukin 6 Homo sapiens 83-87 23199585-7 2013 CAM and AZM induced a dose-dependent suppression of spontaneous TNF-alpha, sTNFR2, IL-6, IL-8 and CCL18 production (p<0.05). Azithromycin 8-11 C-X-C motif chemokine ligand 8 Homo sapiens 89-93 23199585-7 2013 CAM and AZM induced a dose-dependent suppression of spontaneous TNF-alpha, sTNFR2, IL-6, IL-8 and CCL18 production (p<0.05). Azithromycin 8-11 C-C motif chemokine ligand 18 Homo sapiens 98-103 23199585-9 2013 CAM and AZM significantly and dose-dependently attenuated the LPS-stimulated production of sTNFR1, sTNFR2, IL-8 and CCL18 (p<0.05). Azithromycin 8-11 C-X-C motif chemokine ligand 8 Homo sapiens 107-111 23199585-9 2013 CAM and AZM significantly and dose-dependently attenuated the LPS-stimulated production of sTNFR1, sTNFR2, IL-8 and CCL18 (p<0.05). Azithromycin 8-11 C-C motif chemokine ligand 18 Homo sapiens 116-121 23784135-0 2013 Pharmacogenomics of Cytauxzoon felis cytochrome b: implications for atovaquone and azithromycin therapy in domestic cats with cytauxzoonosis. Azithromycin 83-95 cytochrome b Felis catus 37-49 23527897-4 2013 MATERIALS AND METHODS: Employing the standard patch-clamp whole-cell recording technique in murine thymocytes, we examined the effects of 30 and 100 microM clarithromycin and azithromycin on the Kv1.3-channel currents and the membrane capacitance. Azithromycin 175-187 potassium voltage-gated channel, shaker-related subfamily, member 3 Mus musculus 195-200 23546223-2 2013 The macrolide antibiotics including concanamycin A, erythromycin (EM), clarithromycin (CAM) and azithromycin (AZM) all blocked autophagy flux, as assessed by intracellular accumulation of LC3B-II and p62. Azithromycin 96-108 nucleoporin 62 Mus musculus 200-203 23546223-2 2013 The macrolide antibiotics including concanamycin A, erythromycin (EM), clarithromycin (CAM) and azithromycin (AZM) all blocked autophagy flux, as assessed by intracellular accumulation of LC3B-II and p62. Azithromycin 110-113 nucleoporin 62 Mus musculus 200-203 23190027-0 2013 The antibiotic azithromycin is a motilin receptor agonist in human stomach: comparison with erythromycin. Azithromycin 15-27 motilin receptor Homo sapiens 33-49 23065774-7 2013 mRNA and protein expression of key osteoclast transcription factor Nuclear Factor of Activated T cells (NFATc1) was significantly reduced by azithromycin at later stages of osteoclast development (day 17). Azithromycin 141-153 nuclear factor of activated T cells 1 Homo sapiens 104-110 23065774-8 2013 Azithromycin also reduced tumor necrosis factor receptor associated factor-6 (TRAF6) mRNA expression at day 14, and cathepsin K mRNA expression at days 14 and 17. Azithromycin 0-12 TNF receptor associated factor 6 Homo sapiens 26-76 23065774-8 2013 Azithromycin also reduced tumor necrosis factor receptor associated factor-6 (TRAF6) mRNA expression at day 14, and cathepsin K mRNA expression at days 14 and 17. Azithromycin 0-12 TNF receptor associated factor 6 Homo sapiens 78-83 23065774-9 2013 Integrin beta3 and MMP-9 mRNA expression was reduced by azithromycin at day 17 in osteoclasts cultured on dentine. Azithromycin 56-68 integrin subunit beta 3 Homo sapiens 0-14 23065774-9 2013 Integrin beta3 and MMP-9 mRNA expression was reduced by azithromycin at day 17 in osteoclasts cultured on dentine. Azithromycin 56-68 matrix metallopeptidase 9 Homo sapiens 19-24 23577619-5 2013 One candidate being evaluated for IPTp is a fixed-dose combination of azithromycin and chloroquine (AZCQ). Azithromycin 70-82 tRNA isopentenyltransferase 1 Homo sapiens 34-38 23190027-6 2013 KEY RESULTS: Azithromycin (1-100 muM) and erythromycin (3-30 muM) concentration-dependently displaced [(125)I]-motilin binding to the motilin receptor (52 +- 7 and 58 +- 18% displacement at 100 and 30 muM respectively). Azithromycin 13-25 latexin Homo sapiens 33-36 23190027-6 2013 KEY RESULTS: Azithromycin (1-100 muM) and erythromycin (3-30 muM) concentration-dependently displaced [(125)I]-motilin binding to the motilin receptor (52 +- 7 and 58 +- 18% displacement at 100 and 30 muM respectively). Azithromycin 13-25 motilin receptor Homo sapiens 134-150 23190027-7 2013 Azithromycin, erythromycin and motilin concentration-dependently caused short-lived increases in intracellular [Ca(2+)] in cells expressing the motilin receptor. Azithromycin 0-12 motilin receptor Homo sapiens 144-160 23190027-10 2013 Azithromycin and erythromycin lactobionate (30-300 muM each) facilitated these contractions (apparent E(max) values of 2007 +- 396 and 1924 +- 1375%, n = 3-4 each concentration, respectively). Azithromycin 0-12 latexin Homo sapiens 51-54 23291349-9 2013 In a predefined subgroup analysis according to the inflammatory phenotype, azithromycin was associated with a significantly lower PEP rate than placebo in subjects with non-eosinophilic severe asthma (blood eosinophilia <=200/microl): 0.44 PEPs (95% CI 0.25 to 0.78) versus 1.03 PEPs (95% CI 0.72 to 1.48) (p=0.013). Azithromycin 75-87 progestagen associated endometrial protein Homo sapiens 130-133 23248239-0 2013 Azithromycin increases in vitro fibronectin production through interactions between macrophages and fibroblasts stimulated with Pseudomonas aeruginosa. Azithromycin 0-12 fibronectin 1 Mus musculus 32-43 23248239-8 2013 Neutralization of active TGFbeta resulted in the ablation of azithromycin"s ability to increase fibronectin concentrations, but did not alter its ability to increase MMP-9 expression. Azithromycin 61-73 fibronectin 1 Mus musculus 96-107 23248239-9 2013 In P. aeruginosa-infected mice, azithromycin significantly decreased MMP-9 and fibronectin concentrations in the alveolar space compared with non-treated, infected controls. Azithromycin 32-44 matrix metallopeptidase 9 Mus musculus 69-74 23248239-9 2013 In P. aeruginosa-infected mice, azithromycin significantly decreased MMP-9 and fibronectin concentrations in the alveolar space compared with non-treated, infected controls. Azithromycin 32-44 fibronectin 1 Mus musculus 79-90 23248239-10 2013 CONCLUSIONS: Our results suggest that azithromycin"s effect on MMP-9 is regulated independently of TGFbeta activity. Azithromycin 38-50 matrix metallopeptidase 9 Mus musculus 63-68 23248239-11 2013 Additionally, the beneficial effects of azithromycin may be partially due to effects on homeostasis in which ECM-degrading mediators like MMP-9 are up-regulated early after infection. Azithromycin 40-52 matrix metallopeptidase 9 Mus musculus 138-143 23415729-10 2013 Azithromycin reduced both %BAL neutrophilia and IL-17+ cells (both p = 0.016) in the LB group. Azithromycin 0-12 interleukin 17A Homo sapiens 48-53 23415729-13 2013 Moreover, azithromycin significantly decreased the number of IL-17+ cells in the airway wall, which may further explain its effect on BAL neutrophilia. Azithromycin 10-22 interleukin 17A Homo sapiens 61-66 23291349-13 2013 However, the significant reduction in the PEP rate in azithromycin-treated patients with non-eosinophilic severe asthma warrants further study. Azithromycin 54-66 progestagen associated endometrial protein Homo sapiens 42-45 23378729-12 2013 MMP-2 gene expression showed a tendency to decrease in the azithromycin group (p=0.063). Azithromycin 59-71 matrix metallopeptidase 2 Rattus norvegicus 0-5 23462295-10 2013 Azithromycin treatment, prior to LPS priming, further reduced serum TNFalpha and CCL5, yielding the greatest inhibition when the macrolide was also given prior to LPS challenge. Azithromycin 0-12 tumor necrosis factor Mus musculus 68-76 23462295-10 2013 Azithromycin treatment, prior to LPS priming, further reduced serum TNFalpha and CCL5, yielding the greatest inhibition when the macrolide was also given prior to LPS challenge. Azithromycin 0-12 chemokine (C-C motif) ligand 5 Mus musculus 81-85 23421781-0 2013 Bronchiectasis exacerbation study on azithromycin and amoxycillin-clavulanate for respiratory exacerbations in children (BEST-2): study protocol for a randomized controlled trial. Azithromycin 37-49 bestrophin 2 Homo sapiens 121-127 23379441-5 2013 We recently demonstrated in vitro that azithromycin, a macrolide antibiotic, also acts as a nuclear factor (NF)-kappaB inhibitor of murine DCs and inhibits their maturation and functions, including allogeneic responses. Azithromycin 39-51 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 92-118 24371377-0 2013 Azithromycin prevents pregnancy loss: reducing the level of tumor necrosis factor-alpha and raising the level of interleukin-10 in rats. Azithromycin 0-12 tumor necrosis factor Rattus norvegicus 60-87 24371377-0 2013 Azithromycin prevents pregnancy loss: reducing the level of tumor necrosis factor-alpha and raising the level of interleukin-10 in rats. Azithromycin 0-12 interleukin 10 Rattus norvegicus 113-127 24371377-7 2013 Higher TNF- alpha and IL-10 levels were measured (P < 0.05) in the LPS and azithromycin + LPS groups, respectively. Azithromycin 78-90 tumor necrosis factor Rattus norvegicus 7-17 24371377-7 2013 Higher TNF- alpha and IL-10 levels were measured (P < 0.05) in the LPS and azithromycin + LPS groups, respectively. Azithromycin 78-90 interleukin 10 Rattus norvegicus 22-27 23516588-9 2013 Moreover, AZM strongly inhibited the release of Stx2c from E32511 in vitro. Azithromycin 10-13 syntaxin 2 Homo sapiens 48-53 22766066-7 2012 Meanwhile, as compared to naringin, both SP600125 and azithromycin were less effective in suppressing EGF-induced secretion of MUC5AC because of the unchanged nucleus NF-kappaB p65. Azithromycin 54-66 epidermal growth factor Homo sapiens 102-105 24213508-5 2012 The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1. Azithromycin 25-28 collagen type XI alpha 2 chain Homo sapiens 130-134 24213508-5 2012 The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1. Azithromycin 25-28 caspase 3 Homo sapiens 139-148 24213508-5 2012 The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1. Azithromycin 25-28 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 216-221 24213508-5 2012 The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1. Azithromycin 25-28 BCL2 apoptosis regulator Homo sapiens 223-228 23142353-12 2012 Partners treatment with azithromycin improves the 4 months bacteriologic results (EL2). Azithromycin 24-36 spectrin alpha, erythrocytic 1 Homo sapiens 82-85 22766077-6 2012 Further comparison revealed that in LPS-stimulated J774A.1 cells, the cPLA2 inhibitor showed the same profile of inhibition as azithromycin in inhibiting PGE2, IL-6, IL-12p40 and arachidonic acid release. Azithromycin 127-139 interleukin 6 Mus musculus 160-164 22766077-6 2012 Further comparison revealed that in LPS-stimulated J774A.1 cells, the cPLA2 inhibitor showed the same profile of inhibition as azithromycin in inhibiting PGE2, IL-6, IL-12p40 and arachidonic acid release. Azithromycin 127-139 interleukin 12b Mus musculus 166-174 22766077-7 2012 Therefore, we propose that the anti-inflammatory activity of azithromycin in this model may be due to interactions with cPLA2, causing inadequate translocation of the enzyme or disturbing physical interactions with its substrates. Azithromycin 61-73 phospholipase A2, group IVA (cytosolic, calcium-dependent) Mus musculus 120-125 22324488-1 2012 BACKGROUND: This study examines the efficacy of azithromycin in combination with non-surgical periodontal therapy on clinical and microbiologic parameters and gingival crevicular fluid (GCF) matrix metalloproteinases-8 (MMP-8) levels over 6 months in patients with severe generalized chronic periodontitis (CP). Azithromycin 48-60 matrix metallopeptidase 8 Homo sapiens 220-225 22324488-10 2012 The azithromycin and placebo groups exhibited significant reduction in GCF MMP-8 levels at the post-treatment visit and at 2 weeks (P <0.05). Azithromycin 4-16 matrix metallopeptidase 8 Homo sapiens 75-80 22766066-7 2012 Meanwhile, as compared to naringin, both SP600125 and azithromycin were less effective in suppressing EGF-induced secretion of MUC5AC because of the unchanged nucleus NF-kappaB p65. Azithromycin 54-66 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 127-133 23099154-6 2012 Therefore, impairment of lysosomal functions by azithromycin and chloroquine deregulate TLR4 recycling and signaling and phospholipases activation and lead to anti-inflammatory phenotype in LPS-stimulated J774A.1 cells. Azithromycin 48-60 toll-like receptor 4 Mus musculus 88-92 21848430-8 2012 We observed inhibition of cytokines (interleukin [IL]-1beta (beta), IL-6, IL-8, IL-10, and tumor necrosis factor-alpha) in the presence of azithromycin in EB-stimulated cells from both fertile and infertile women with primary and recurrent C. trachomatis infection. Azithromycin 139-151 interleukin 6 Homo sapiens 68-72 22410149-6 2012 However, AZM did show a dose-dependent suppression on IL-15-induced CD69 expression of primary NK cells. Azithromycin 9-12 interleukin 15 Homo sapiens 54-59 22410149-6 2012 However, AZM did show a dose-dependent suppression on IL-15-induced CD69 expression of primary NK cells. Azithromycin 9-12 CD69 molecule Homo sapiens 68-72 22410149-7 2012 AZM inhibited the cytotoxicity against K562 cells of resting and IL-15 activated primary NK cells possibly through down-regulation of perforin expression, especially on CD16(+)CD56(+) NK subsets. Azithromycin 0-3 interleukin 15 Homo sapiens 65-70 22410149-7 2012 AZM inhibited the cytotoxicity against K562 cells of resting and IL-15 activated primary NK cells possibly through down-regulation of perforin expression, especially on CD16(+)CD56(+) NK subsets. Azithromycin 0-3 Fc gamma receptor IIIa Homo sapiens 169-173 22410149-7 2012 AZM inhibited the cytotoxicity against K562 cells of resting and IL-15 activated primary NK cells possibly through down-regulation of perforin expression, especially on CD16(+)CD56(+) NK subsets. Azithromycin 0-3 neural cell adhesion molecule 1 Homo sapiens 176-180 22410149-8 2012 AZM exerted a dose-dependent inhibition of IFN-gamma and TNF-alpha production from NK-92 cells, but did not affect the cytokine production of IL-15 activated primary NK cells. Azithromycin 0-3 interferon gamma Homo sapiens 43-52 22410149-8 2012 AZM exerted a dose-dependent inhibition of IFN-gamma and TNF-alpha production from NK-92 cells, but did not affect the cytokine production of IL-15 activated primary NK cells. Azithromycin 0-3 tumor necrosis factor Homo sapiens 57-66 21726210-6 2012 KEY RESULTS: Azithromycin (1.5-50 microM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-alpha or IL-6. Azithromycin 13-25 C-C motif chemokine receptor 7 Homo sapiens 126-130 21726210-6 2012 KEY RESULTS: Azithromycin (1.5-50 microM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-alpha or IL-6. Azithromycin 13-25 C-X-C motif chemokine ligand 11 Homo sapiens 132-139 21726210-6 2012 KEY RESULTS: Azithromycin (1.5-50 microM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-alpha or IL-6. Azithromycin 13-25 C-C motif chemokine ligand 2 Homo sapiens 168-172 21726210-6 2012 KEY RESULTS: Azithromycin (1.5-50 microM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-alpha or IL-6. Azithromycin 13-25 tumor necrosis factor Homo sapiens 191-200 21726210-6 2012 KEY RESULTS: Azithromycin (1.5-50 microM) dose-dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL-12p70), but enhanced CCL2, without altering TNF-alpha or IL-6. Azithromycin 13-25 interleukin 6 Homo sapiens 204-208 21726210-7 2012 Azithromycin also enhanced the gene expression and/or release of M2 macrophage markers (IL-10 and CCL18), and the pan-monocyte marker CD163, but inhibited that of CCL22. Azithromycin 0-12 interleukin 10 Homo sapiens 88-93 21726210-7 2012 Azithromycin also enhanced the gene expression and/or release of M2 macrophage markers (IL-10 and CCL18), and the pan-monocyte marker CD163, but inhibited that of CCL22. Azithromycin 0-12 C-C motif chemokine ligand 18 Homo sapiens 98-103 21726210-7 2012 Azithromycin also enhanced the gene expression and/or release of M2 macrophage markers (IL-10 and CCL18), and the pan-monocyte marker CD163, but inhibited that of CCL22. Azithromycin 0-12 C-C motif chemokine ligand 22 Homo sapiens 163-168 21726210-11 2012 CONCLUSIONS AND IMPLICATIONS: Azithromycin modulated classical activation of human monocytes by inhibition of TLR4-mediated signalling and possible effects on lysosomal function, and generated a mediator expression profile that differs from that of monocyte/macrophage phenotypes so far described. Azithromycin 30-42 toll like receptor 4 Homo sapiens 110-114 22677362-4 2012 The tested macrolides, clarithromycin and azithromycin, administered orally (2 x 150 mg/kg) 0.5 h before and 5 h after cantharidin challenge, reduced MIP-2, MCP-1, KC, and MPO concentrations and thereby decreased ear swelling. Azithromycin 42-54 chemokine (C-X-C motif) ligand 2 Mus musculus 150-155 22677362-4 2012 The tested macrolides, clarithromycin and azithromycin, administered orally (2 x 150 mg/kg) 0.5 h before and 5 h after cantharidin challenge, reduced MIP-2, MCP-1, KC, and MPO concentrations and thereby decreased ear swelling. Azithromycin 42-54 chemokine (C-C motif) ligand 2 Mus musculus 157-162 22677362-4 2012 The tested macrolides, clarithromycin and azithromycin, administered orally (2 x 150 mg/kg) 0.5 h before and 5 h after cantharidin challenge, reduced MIP-2, MCP-1, KC, and MPO concentrations and thereby decreased ear swelling. Azithromycin 42-54 myeloperoxidase Mus musculus 172-175 22471971-14 2012 TRIAL REGISTRATION: Current Controlled Trials NTR 2555 MEC AZM/UM: NL 31988.068.10 / MEC 10-3-052. Azithromycin 59-62 neurotensin receptor 1 Homo sapiens 46-49 22471971-14 2012 TRIAL REGISTRATION: Current Controlled Trials NTR 2555 MEC AZM/UM: NL 31988.068.10 / MEC 10-3-052. Azithromycin 59-62 C-C motif chemokine ligand 28 Homo sapiens 55-58 22471971-14 2012 TRIAL REGISTRATION: Current Controlled Trials NTR 2555 MEC AZM/UM: NL 31988.068.10 / MEC 10-3-052. Azithromycin 59-62 C-C motif chemokine ligand 28 Homo sapiens 85-88 21848430-8 2012 We observed inhibition of cytokines (interleukin [IL]-1beta (beta), IL-6, IL-8, IL-10, and tumor necrosis factor-alpha) in the presence of azithromycin in EB-stimulated cells from both fertile and infertile women with primary and recurrent C. trachomatis infection. Azithromycin 139-151 C-X-C motif chemokine ligand 8 Homo sapiens 74-78 21848430-8 2012 We observed inhibition of cytokines (interleukin [IL]-1beta (beta), IL-6, IL-8, IL-10, and tumor necrosis factor-alpha) in the presence of azithromycin in EB-stimulated cells from both fertile and infertile women with primary and recurrent C. trachomatis infection. Azithromycin 139-151 interleukin 10 Homo sapiens 80-85 21848430-8 2012 We observed inhibition of cytokines (interleukin [IL]-1beta (beta), IL-6, IL-8, IL-10, and tumor necrosis factor-alpha) in the presence of azithromycin in EB-stimulated cells from both fertile and infertile women with primary and recurrent C. trachomatis infection. Azithromycin 139-151 tumor necrosis factor Homo sapiens 91-118 21336676-6 2012 In OXA-induced chronic DTH, azithromycin (1 mg/ear) reduced the number of ear tissue mast cells and decreased the concentration of IL-4 in ear tissue and of immunoglobulin (Ig)E in serum. Azithromycin 28-40 interleukin 4 Mus musculus 131-135 22490409-0 2012 Azithromycin inhibits neutrophil accumulation in airways by affecting interleukin-17 downstream signals. Azithromycin 0-12 interleukin 17A Mus musculus 70-84 22490409-3 2012 Our experiment assessed whether azithromycin inhibits neutrophil accumulation in the airways by affecting interleukin-17 (IL-17) downstream signals. Azithromycin 32-44 interleukin 17A Mus musculus 106-120 22490409-3 2012 Our experiment assessed whether azithromycin inhibits neutrophil accumulation in the airways by affecting interleukin-17 (IL-17) downstream signals. Azithromycin 32-44 interleukin 17A Mus musculus 122-127 22490409-7 2012 RESULTS: (1) Azithromycin pretreatment significantly inhibited both the release of three neutrophil-mobilizing cytokines (MIP-2, CXCL-5 and GM-CSF) and the accumulation of neutrophils in airways caused by mIL-17 stimulation. Azithromycin 13-25 chemokine (C-X-C motif) ligand 2 Mus musculus 122-127 22490409-7 2012 RESULTS: (1) Azithromycin pretreatment significantly inhibited both the release of three neutrophil-mobilizing cytokines (MIP-2, CXCL-5 and GM-CSF) and the accumulation of neutrophils in airways caused by mIL-17 stimulation. Azithromycin 13-25 chemokine (C-X-C motif) ligand 5 Mus musculus 129-135 22490409-7 2012 RESULTS: (1) Azithromycin pretreatment significantly inhibited both the release of three neutrophil-mobilizing cytokines (MIP-2, CXCL-5 and GM-CSF) and the accumulation of neutrophils in airways caused by mIL-17 stimulation. Azithromycin 13-25 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 140-146 22490409-7 2012 RESULTS: (1) Azithromycin pretreatment significantly inhibited both the release of three neutrophil-mobilizing cytokines (MIP-2, CXCL-5 and GM-CSF) and the accumulation of neutrophils in airways caused by mIL-17 stimulation. Azithromycin 13-25 interleukin 17A Mus musculus 205-211 22490409-9 2012 CONCLUSIONS: Azithromycin can inhibit neutrophil accumulation in the airways by affecting IL-17 downstream signals. Azithromycin 13-25 interleukin 17A Mus musculus 90-95 21336676-0 2012 Topical azithromycin and clarithromycin inhibit acute and chronic skin inflammation in sensitized mice, with apparent selectivity for Th2-mediated processes in delayed-type hypersensitivity. Azithromycin 8-20 heart and neural crest derivatives expressed 2 Mus musculus 134-137 21336676-3 2012 Dexamethasone (50 mug/ear), azithromycin, and clarithromycin (500 mug/ear) reduced TNF-alpha and interleukin (IL)-1beta concentration in ear tissue by inhibiting inflammatory cell accumulation in PMA-induced inflammation. Azithromycin 28-40 tumor necrosis factor Mus musculus 83-92 21336676-3 2012 Dexamethasone (50 mug/ear), azithromycin, and clarithromycin (500 mug/ear) reduced TNF-alpha and interleukin (IL)-1beta concentration in ear tissue by inhibiting inflammatory cell accumulation in PMA-induced inflammation. Azithromycin 28-40 interleukin 1 beta Mus musculus 97-119 21336676-8 2012 In conclusion, azithromycin and clarithromycin attenuate pro-inflammatory cytokine production and leukocyte infiltration during innate immune reactions, while selectively affecting Th2 rather than Th1 immunity in DTH reactions. Azithromycin 15-27 heart and neural crest derivatives expressed 2 Mus musculus 181-184 21336676-8 2012 In conclusion, azithromycin and clarithromycin attenuate pro-inflammatory cytokine production and leukocyte infiltration during innate immune reactions, while selectively affecting Th2 rather than Th1 immunity in DTH reactions. Azithromycin 15-27 negative elongation factor complex member C/D, Th1l Mus musculus 197-200 22993937-3 2012 The treatment with azithromycin, in addition to the high eradication rates, was also evident of its effect on the cytokine levels in the patients, that was characteristic of a significant increase of the IFN-gamma level and a decrease of the IL-1beta and IL-6 levels in the blood. Azithromycin 19-31 interferon gamma Homo sapiens 204-213 22131344-0 2012 Azithromycin drives in vitro GM-CSF/IL-4-induced differentiation of human blood monocytes toward dendritic-like cells with regulatory properties. Azithromycin 0-12 colony stimulating factor 2 Homo sapiens 29-35 22131344-0 2012 Azithromycin drives in vitro GM-CSF/IL-4-induced differentiation of human blood monocytes toward dendritic-like cells with regulatory properties. Azithromycin 0-12 interleukin 4 Homo sapiens 36-40 22131344-7 2012 Azithromycin, added 2 h before activation of iDCs with LPS, enhanced IL-10 release and inhibited IL-6, IL-12p40, CXCL10, CXCL11, and CCL22 release. Azithromycin 0-12 interleukin 10 Homo sapiens 69-74 22131344-7 2012 Azithromycin, added 2 h before activation of iDCs with LPS, enhanced IL-10 release and inhibited IL-6, IL-12p40, CXCL10, CXCL11, and CCL22 release. Azithromycin 0-12 interleukin 6 Homo sapiens 97-101 22131344-7 2012 Azithromycin, added 2 h before activation of iDCs with LPS, enhanced IL-10 release and inhibited IL-6, IL-12p40, CXCL10, CXCL11, and CCL22 release. Azithromycin 0-12 C-X-C motif chemokine ligand 10 Homo sapiens 113-119 22131344-7 2012 Azithromycin, added 2 h before activation of iDCs with LPS, enhanced IL-10 release and inhibited IL-6, IL-12p40, CXCL10, CXCL11, and CCL22 release. Azithromycin 0-12 C-X-C motif chemokine ligand 11 Homo sapiens 121-127 22131344-7 2012 Azithromycin, added 2 h before activation of iDCs with LPS, enhanced IL-10 release and inhibited IL-6, IL-12p40, CXCL10, CXCL11, and CCL22 release. Azithromycin 0-12 C-C motif chemokine ligand 22 Homo sapiens 133-138 22993937-3 2012 The treatment with azithromycin, in addition to the high eradication rates, was also evident of its effect on the cytokine levels in the patients, that was characteristic of a significant increase of the IFN-gamma level and a decrease of the IL-1beta and IL-6 levels in the blood. Azithromycin 19-31 interleukin 1 beta Homo sapiens 242-250 22993937-3 2012 The treatment with azithromycin, in addition to the high eradication rates, was also evident of its effect on the cytokine levels in the patients, that was characteristic of a significant increase of the IFN-gamma level and a decrease of the IL-1beta and IL-6 levels in the blood. Azithromycin 19-31 interleukin 6 Homo sapiens 255-259 22699716-0 2012 Azithromycin pulses for the treatment of epidermal growth factor receptor inhibitor-related papulopustular eruption: an effective and convenient alternative to tetracyclines. Azithromycin 0-12 epidermal growth factor receptor Homo sapiens 41-73 23226013-3 2012 METHODS: Participants in a study designed to determine if azithromycin taken daily for one year decreased acute exacerbations had serum mannose-binding lectin concentrations measured at the time of enrollment. Azithromycin 58-70 mannose binding lectin 2 Homo sapiens 136-158 23284981-3 2012 Here we determined if regional variation in the EMT response to TGFbeta1 underlies the bronchiolocentric fibrosis leading to BOS and whether EMT could be inhibited by azithromycin or mycophenolate. Azithromycin 167-179 IL2 inducible T cell kinase Homo sapiens 141-144 22577246-5 2012 AZM or CAM significantly inhibited tumor necrosis factor-alpha (TNF-alpha) (20 ng/mL)-induced MUC5AC secretion from NCI-H292 cells at 10-6-10-7 M, whereas JM or ABPC showed no effect. Azithromycin 0-3 tumor necrosis factor Homo sapiens 35-62 22577246-5 2012 AZM or CAM significantly inhibited tumor necrosis factor-alpha (TNF-alpha) (20 ng/mL)-induced MUC5AC secretion from NCI-H292 cells at 10-6-10-7 M, whereas JM or ABPC showed no effect. Azithromycin 0-3 tumor necrosis factor Homo sapiens 64-73 22577246-5 2012 AZM or CAM significantly inhibited tumor necrosis factor-alpha (TNF-alpha) (20 ng/mL)-induced MUC5AC secretion from NCI-H292 cells at 10-6-10-7 M, whereas JM or ABPC showed no effect. Azithromycin 0-3 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 94-100 22577246-6 2012 AZM significantly inhibited TNF-alpha (20 ng/mL)-induced MUC5AC secretion from human nasal epithelial cells at 10-4 M. MUC5AC mRNA expression was also significantly inhibited. Azithromycin 0-3 tumor necrosis factor Homo sapiens 28-37 22577246-6 2012 AZM significantly inhibited TNF-alpha (20 ng/mL)-induced MUC5AC secretion from human nasal epithelial cells at 10-4 M. MUC5AC mRNA expression was also significantly inhibited. Azithromycin 0-3 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 57-63 22577246-6 2012 AZM significantly inhibited TNF-alpha (20 ng/mL)-induced MUC5AC secretion from human nasal epithelial cells at 10-4 M. MUC5AC mRNA expression was also significantly inhibited. Azithromycin 0-3 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 119-125 23284981-6 2012 Azithromycin potentially inhibited EMT in both small and large airway epithelial cells by inhibiting Smad3 expression, but not activation. Azithromycin 0-12 IL2 inducible T cell kinase Homo sapiens 35-38 23284981-6 2012 Azithromycin potentially inhibited EMT in both small and large airway epithelial cells by inhibiting Smad3 expression, but not activation. Azithromycin 0-12 SMAD family member 3 Homo sapiens 101-106 22150046-0 2011 Azithromycin for prevention of exacerbations of COPD. Azithromycin 0-12 COPD Homo sapiens 48-52 22150045-0 2011 Azithromycin for prevention of exacerbations of COPD. Azithromycin 0-12 COPD Homo sapiens 48-52 22150047-0 2011 Azithromycin for prevention of exacerbations of COPD. Azithromycin 0-12 COPD Homo sapiens 48-52 22150048-0 2011 Azithromycin for prevention of exacerbations of COPD. Azithromycin 0-12 COPD Homo sapiens 48-52 22063535-1 2011 An electrochemical method has been successfully demonstrated for sensitive determination of azithromycin (Azi) with room temperature ionic liquid (IL) of 1-butyl-3-methylimidazolium hexafluorophosphate (BMIMPF(6)) - graphene (Gr) composite modified glassy carbon electrode (GCE). Azithromycin 92-104 glycine decarboxylase Homo sapiens 274-277 22059997-5 2011 A comparative in vitro study of five clinically used drugs that are known to inhibit NF-kappaB demonstrated that azithromycin, a macrolide antibiotic, significantly inhibited expression of co-stimulatory molecules (CD40 and CD86) and major histocompatibility complex (MHC) class II by DCs. Azithromycin 113-125 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 85-94 22059997-5 2011 A comparative in vitro study of five clinically used drugs that are known to inhibit NF-kappaB demonstrated that azithromycin, a macrolide antibiotic, significantly inhibited expression of co-stimulatory molecules (CD40 and CD86) and major histocompatibility complex (MHC) class II by DCs. Azithromycin 113-125 CD40 antigen Mus musculus 215-219 22059997-5 2011 A comparative in vitro study of five clinically used drugs that are known to inhibit NF-kappaB demonstrated that azithromycin, a macrolide antibiotic, significantly inhibited expression of co-stimulatory molecules (CD40 and CD86) and major histocompatibility complex (MHC) class II by DCs. Azithromycin 113-125 CD86 antigen Mus musculus 224-228 22059997-7 2011 These data suggest that azithromycin, as not only an NF-kappaB inhibitor but also an antibiotic, has potential as a novel drug for manipulation of allogeneic responses. Azithromycin 24-36 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 53-62 21417583-4 2011 Therefore, we investigated the effects of AZM on IL-8 production in an oral epithelial cell line. Azithromycin 42-45 C-X-C motif chemokine ligand 8 Homo sapiens 49-53 21417583-8 2011 RESULTS: IL-8 mRNA expression, IL-8 production, and NF-kappaB activation in LPS-stimulated KB cells were inhibited by the addition of AZM. Azithromycin 134-137 C-X-C motif chemokine ligand 8 Homo sapiens 9-13 21417583-8 2011 RESULTS: IL-8 mRNA expression, IL-8 production, and NF-kappaB activation in LPS-stimulated KB cells were inhibited by the addition of AZM. Azithromycin 134-137 C-X-C motif chemokine ligand 8 Homo sapiens 31-35 21417583-10 2011 CONCLUSIONS: This study suggests that AZM inhibits LPS-induced IL-8 production in an oral epithelial cell line, in part caused by the suppression of Rac1 and NF-kappaB activation. Azithromycin 38-41 C-X-C motif chemokine ligand 8 Homo sapiens 63-67 22063535-1 2011 An electrochemical method has been successfully demonstrated for sensitive determination of azithromycin (Azi) with room temperature ionic liquid (IL) of 1-butyl-3-methylimidazolium hexafluorophosphate (BMIMPF(6)) - graphene (Gr) composite modified glassy carbon electrode (GCE). Azithromycin 106-109 glycine decarboxylase Homo sapiens 274-277 22063535-2 2011 The cyclic voltammetric results indicate that Gr/IL/GCE can remarkably enhance electrocatalytic activity towards the oxidation of Azi in neutral solutions. Azithromycin 130-133 glycine decarboxylase Homo sapiens 46-55 21507332-0 2011 Azithromycin acts as an immunomodulatory agent to suppress the expression of TREM-1 in Bacillus pyocyaneus-induced sepsis. Azithromycin 0-12 triggering receptor expressed on myeloid cells 1 Homo sapiens 77-83 21812004-4 2011 MDR1 substrates reduced the basolateral-to-apical transport of CAM and AZM. Azithromycin 71-74 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 0-4 21812004-7 2011 These data suggest that the high distribution of CAM and AZM to AMs is due to the sustained distribution to ELF via MDR1 as well as the high uptake by the AMs themselves via active transport mechanisms. Azithromycin 57-60 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 116-120 21899548-10 2011 The stimulation of PBMCs with concanavalin A or TSST-1 increased cellular JNK and ERK activity, and 5 microg/ml azithromycin significantly attenuated the increased activity of JNK in the TSST-1-stimulated cells and ERK in the concanavalin A- and TSST-1-stimulated PBMCs, respectively (P < 0.05). Azithromycin 112-124 mitogen-activated protein kinase 1 Homo sapiens 215-218 21899548-11 2011 CONCLUSIONS: Azithromycin suppresses mitogen- or superantigen-induced proliferation of PBMCs by possibly inhibiting both cellular JNK and ERK activity. Azithromycin 13-25 mitogen-activated protein kinase 8 Homo sapiens 130-133 21899548-11 2011 CONCLUSIONS: Azithromycin suppresses mitogen- or superantigen-induced proliferation of PBMCs by possibly inhibiting both cellular JNK and ERK activity. Azithromycin 13-25 mitogen-activated protein kinase 1 Homo sapiens 138-141 21740970-0 2011 Azithromycin decreases MMP-9 expression in the airways of lung transplant recipients. Azithromycin 0-12 matrix metallopeptidase 9 Homo sapiens 23-28 21740970-11 2011 Although azithromycin significantly reduced ELISA MMP-9 levels and gelatinolytic activity in transplant patients, these levels remained higher compared to control patients (p=0.0011 and p=0.043). Azithromycin 9-21 matrix metallopeptidase 9 Homo sapiens 50-55 21908042-7 2011 The infection induced up-regulation of the macrophage migration inhibitory factor (MIF), which was also enhanced in infected cells after treatment with azithromycin, but not with spiramycin. Azithromycin 152-164 macrophage migration inhibitory factor Homo sapiens 43-81 21908042-7 2011 The infection induced up-regulation of the macrophage migration inhibitory factor (MIF), which was also enhanced in infected cells after treatment with azithromycin, but not with spiramycin. Azithromycin 152-164 macrophage migration inhibitory factor Homo sapiens 83-86 21899548-9 2011 The concentrations of TNF-alpha, interleukin (IL)-2, -4, -5 and -10 in the supernatant of concanavalin A- or TSST-1-stimulated PBMCs cultured for 72 h decreased by 65-98% in the presence of 5 microg/ml azithromycin. Azithromycin 202-214 tumor necrosis factor Homo sapiens 22-31 21899548-9 2011 The concentrations of TNF-alpha, interleukin (IL)-2, -4, -5 and -10 in the supernatant of concanavalin A- or TSST-1-stimulated PBMCs cultured for 72 h decreased by 65-98% in the presence of 5 microg/ml azithromycin. Azithromycin 202-214 interleukin 2 Homo sapiens 33-67 21899548-10 2011 The stimulation of PBMCs with concanavalin A or TSST-1 increased cellular JNK and ERK activity, and 5 microg/ml azithromycin significantly attenuated the increased activity of JNK in the TSST-1-stimulated cells and ERK in the concanavalin A- and TSST-1-stimulated PBMCs, respectively (P < 0.05). Azithromycin 112-124 mitogen-activated protein kinase 8 Homo sapiens 74-77 21899548-10 2011 The stimulation of PBMCs with concanavalin A or TSST-1 increased cellular JNK and ERK activity, and 5 microg/ml azithromycin significantly attenuated the increased activity of JNK in the TSST-1-stimulated cells and ERK in the concanavalin A- and TSST-1-stimulated PBMCs, respectively (P < 0.05). Azithromycin 112-124 mitogen-activated protein kinase 8 Homo sapiens 176-179 21507332-3 2011 The purpose of the current study was to determine whether azithromycin, a type of macrolide antibiotic, could reduce the expression of TREM-1 in Bacillus pyocyaneus-induced sepsis in vitro and in vivo. Azithromycin 58-70 triggering receptor expressed on myeloid cells 1 Homo sapiens 135-141 21507332-9 2011 However, treatment with TREM-1/Fc fusion protein or azithromycin reduced the effect of LPS-stimulated TREM-1 protein expression. Azithromycin 52-64 triggering receptor expressed on myeloid cells 1 Homo sapiens 102-108 21597298-0 2011 Azithromycin inhibits IL-5 production of T helper type 2 cells from asthmatic children. Azithromycin 0-12 interleukin 5 Homo sapiens 22-26 21628536-8 2011 Preincubation of Chang and human corneal limbal epithelial cells with AZM, ERY, and TET at >=64 mug/ml provided protection against AZM-susceptible S. aureus strains, with increasing protection at higher concentrations. Azithromycin 134-137 tetracycline-resistance protein Staphylococcus aureus 84-87 21477099-7 2011 We also present the evidence for mefloquine and azithromycin-based combinations (ABCs), two leading drug options to replace SP in IPTp. Azithromycin 48-60 tRNA isopentenyltransferase 1 Homo sapiens 130-134 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 interleukin 1 beta Homo sapiens 142-150 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 interleukin 6 Homo sapiens 152-156 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 interleukin 10 Homo sapiens 158-163 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 tumor necrosis factor Homo sapiens 165-174 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-C motif chemokine ligand 3 Homo sapiens 176-180 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-C motif chemokine ligand 5 Homo sapiens 182-186 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-C motif chemokine ligand 20 Homo sapiens 188-193 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-C motif chemokine ligand 22 Homo sapiens 195-200 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-X-C motif chemokine ligand 1 Homo sapiens 202-207 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 C-X-C motif chemokine ligand 5 Homo sapiens 209-214 21315154-4 2011 Three of the four tested macrolides, azithromycin, clarithromycin and roxithromycin, exhibited pronounced, concentration-related reduction of IL-1beta, IL-6, IL-10, TNF-alpha, CCL3, CCL5, CCL20, CCL22, CXCL1, CXCL5, and G-CSF release. Azithromycin 37-49 colony stimulating factor 3 Homo sapiens 220-225 21296809-11 2011 AZM also significantly decreased messenger RNA expression levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 in the cornea. Azithromycin 0-3 interleukin 1 beta Mus musculus 68-85 21296809-11 2011 AZM also significantly decreased messenger RNA expression levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 in the cornea. Azithromycin 0-3 interleukin 1 beta Mus musculus 87-95 21296809-11 2011 AZM also significantly decreased messenger RNA expression levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 in the cornea. Azithromycin 0-3 tumor necrosis factor Mus musculus 98-125 21296809-11 2011 AZM also significantly decreased messenger RNA expression levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 in the cornea. Azithromycin 0-3 tumor necrosis factor Mus musculus 127-136 21296809-11 2011 AZM also significantly decreased messenger RNA expression levels of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 in the cornea. Azithromycin 0-3 intercellular adhesion molecule 1 Mus musculus 142-148 21296809-14 2011 This was further supported by an associated decrease in expression of IL-1beta, TNF-alpha, and ICAM-1 in the cornea, indicating AZM may have a potential anti-inflammatory effect on corneal inflammation. Azithromycin 128-131 interleukin 1 beta Mus musculus 70-78 21296809-14 2011 This was further supported by an associated decrease in expression of IL-1beta, TNF-alpha, and ICAM-1 in the cornea, indicating AZM may have a potential anti-inflammatory effect on corneal inflammation. Azithromycin 128-131 tumor necrosis factor Mus musculus 80-89 21296809-14 2011 This was further supported by an associated decrease in expression of IL-1beta, TNF-alpha, and ICAM-1 in the cornea, indicating AZM may have a potential anti-inflammatory effect on corneal inflammation. Azithromycin 128-131 intercellular adhesion molecule 1 Mus musculus 95-101 21195124-4 2011 Using immunohistochemistry, mRNA and specific protein assays, we confirmed that azithromycin ameliorates LPS-induced pulmonary neutrophilia by inhibiting interleukin-1beta (IL-1beta) expression and production selectively in alveolar macrophages as well as in LPS-stimulated J774.2 macrophage-derived cells in vitro. Azithromycin 80-92 interleukin 1 beta Mus musculus 154-171 21195124-4 2011 Using immunohistochemistry, mRNA and specific protein assays, we confirmed that azithromycin ameliorates LPS-induced pulmonary neutrophilia by inhibiting interleukin-1beta (IL-1beta) expression and production selectively in alveolar macrophages as well as in LPS-stimulated J774.2 macrophage-derived cells in vitro. Azithromycin 80-92 interleukin 1 beta Mus musculus 173-181 21195124-5 2011 Inhibition by azithromycin of neutrophilia and IL-1beta was accompanied by prevention of nuclear expression of activator protein-1 (AP-1) in both alveolar macrophages and J774.2 cells. Azithromycin 14-26 jun proto-oncogene Mus musculus 111-130 21195124-5 2011 Inhibition by azithromycin of neutrophilia and IL-1beta was accompanied by prevention of nuclear expression of activator protein-1 (AP-1) in both alveolar macrophages and J774.2 cells. Azithromycin 14-26 jun proto-oncogene Mus musculus 132-136 21195124-7 2011 In conclusion, we have shown that inhibition of LPS-induced pulmonary neutrophilia and IL-1beta concentrations in lung tissue following azithromycin treatment is mediated through effects on alveolar macrophages. Azithromycin 136-148 interleukin 1 beta Mus musculus 87-95 21195124-8 2011 In addition, we have shown for the first time, in an in vivo model, that azithromycin inhibits AP-1 activation in alveolar macrophages, an action confirmed on J774.2 cells in vitro. Azithromycin 73-85 jun proto-oncogene Mus musculus 95-99 21600177-0 2011 [Inhibition of airway mucous hypersecretion by azithromycin through matrix metalloproteinase 9]. Azithromycin 47-59 matrix metallopeptidase 9 Homo sapiens 68-94 21600177-1 2011 OBJECTIVE: To investigate the mechanism of azithromycin (AZT) inhibiting the airway mucous hypersecretion through matrix metalloproteinase 9 (MMP9). Azithromycin 43-55 matrix metallopeptidase 9 Homo sapiens 114-140 21600177-1 2011 OBJECTIVE: To investigate the mechanism of azithromycin (AZT) inhibiting the airway mucous hypersecretion through matrix metalloproteinase 9 (MMP9). Azithromycin 43-55 matrix metallopeptidase 9 Homo sapiens 142-146 21600177-1 2011 OBJECTIVE: To investigate the mechanism of azithromycin (AZT) inhibiting the airway mucous hypersecretion through matrix metalloproteinase 9 (MMP9). Azithromycin 57-60 matrix metallopeptidase 9 Homo sapiens 114-140 21600177-1 2011 OBJECTIVE: To investigate the mechanism of azithromycin (AZT) inhibiting the airway mucous hypersecretion through matrix metalloproteinase 9 (MMP9). Azithromycin 57-60 matrix metallopeptidase 9 Homo sapiens 142-146 21600177-14 2011 CONCLUSION: AZT may suppress the activity and production of MMP9 in HBE16 cells so as to inhibit the airway mucous hypersecretion. Azithromycin 12-15 matrix metallopeptidase 9 Homo sapiens 60-64 21864166-0 2011 Azithromycin for prevention of exacerbations of COPD. Azithromycin 0-12 COPD Homo sapiens 48-52 21864166-3 2011 METHODS: We performed a randomized trial to determine whether azithromycin decreased the frequency of exacerbations in participants with COPD who had an increased risk of exacerbations but no hearing impairment, resting tachycardia, or apparent risk of prolongation of the corrected QT interval. Azithromycin 62-74 COPD Homo sapiens 137-141 21864166-7 2011 The frequency of exacerbations was 1.48 exacerbations per patient-year in the azithromycin group, as compared with 1.83 per patient-year in the placebo group (P=0.01), and the hazard ratio for having an acute exacerbation of COPD per patient-year in the azithromycin group was 0.73 (95% CI, 0.63 to 0.84; P<0.001). Azithromycin 78-90 COPD Homo sapiens 225-229 21864166-10 2011 CONCLUSIONS: Among selected subjects with COPD, azithromycin taken daily for 1 year, when added to usual treatment, decreased the frequency of exacerbations and improved quality of life but caused hearing decrements in a small percentage of subjects. Azithromycin 48-60 COPD Homo sapiens 42-46 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Azithromycin 264-276 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21195124-0 2011 Azithromycin inhibits macrophage interleukin-1beta production through inhibition of activator protein-1 in lipopolysaccharide-induced murine pulmonary neutrophilia. Azithromycin 0-12 interleukin 1 beta Mus musculus 33-50 21195124-0 2011 Azithromycin inhibits macrophage interleukin-1beta production through inhibition of activator protein-1 in lipopolysaccharide-induced murine pulmonary neutrophilia. Azithromycin 0-12 jun proto-oncogene Mus musculus 84-103 20562124-9 2011 Patients receiving azithromycin demonstrated better FEV1 (p = 0.028), and lower airway neutrophilia (p = 0.015) and systemic C-reactive protein levels (p = 0.050) over time. Azithromycin 19-31 C-reactive protein Homo sapiens 125-143 20562124-12 2011 Azithromycin prophylaxis attenuates local and systemic inflammation, improves FEV1 and reduces BOS 2 yrs after LTx. Azithromycin 0-12 BOS2 Homo sapiens 95-100 21597298-8 2011 AZM inhibited IL-5 production of Th0 and Th2 cells from atopic asthmatics in a dose-dependent fashion, without significantly affecting their IL-13 and IFN-gamma production. Azithromycin 0-3 interleukin 5 Homo sapiens 14-18 21597298-9 2011 A similar effect was observed in non-atopic controls except that AZM did inhibit IFN-gamma production of their Th0 cells. Azithromycin 65-68 interferon gamma Homo sapiens 81-90 21597298-11 2011 CONCLUSION: Our finding that AZM preferentially downregulates IL-5 production suggests its therapeutic potentials in controlling childhood asthma. Azithromycin 29-32 interleukin 5 Homo sapiens 62-66 21853949-16 2011 CONCLUSIONS: Azithromycin is a comfortable alternative for other topical antibiotics, especially in repetitive procedures like anti-VEGF injections. Azithromycin 13-25 vascular endothelial growth factor A Homo sapiens 132-136 20619258-0 2010 Azithromycin inhibits nontypeable Haemophilus influenzae-induced MUC5AC expression and secretion via inhibition of activator protein-1 in human airway epithelial cells. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 65-71 20538995-8 2010 These stimulated levels of proinflammatory mediators by zymosan were significantly inhibited by TLR2 antibody, NF-kappaB-I, or azithromycin, which blocked zymosan-induced NF-kappaB activation as determined by p65 protein nuclear translocation. Azithromycin 127-139 RELA proto-oncogene, NF-kB subunit Homo sapiens 209-212 20619258-0 2010 Azithromycin inhibits nontypeable Haemophilus influenzae-induced MUC5AC expression and secretion via inhibition of activator protein-1 in human airway epithelial cells. Azithromycin 0-12 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 115-134 20619258-5 2010 A 15-membered macrolide, azithromycin, but not a 14-membered macrolide, clarithromycin, inhibited NTHi-induction of MUC5AC at both the mRNA and protein levels through selective suppression of activation of the transcription factor activator protein-1. Azithromycin 25-37 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 116-122 20619258-5 2010 A 15-membered macrolide, azithromycin, but not a 14-membered macrolide, clarithromycin, inhibited NTHi-induction of MUC5AC at both the mRNA and protein levels through selective suppression of activation of the transcription factor activator protein-1. Azithromycin 25-37 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 231-250 20128647-0 2010 Anti-inflammatory activity of azithromycin as measured by its NF-kappaB, inhibitory activity. Azithromycin 30-42 nuclear factor kappa B subunit 1 Homo sapiens 62-71 21103422-3 2010 An alternative, azithromycin (AZI), lacks P450 inhibition. Azithromycin 16-28 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 42-46 20621639-4 2010 Expression of MDR1 on cells decreased macrolide accumulation in cells from 2- to 80-fold with the most pronounced change observed for azithromycin and erythromycin. Azithromycin 134-146 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 20621639-6 2010 In conclusion, out of seven applied methods and assessed parameters, four of them gave similar rough evaluation on the strength of interaction of five macrolides with MDR1, with clarithromycin, roxithromycin and telithromycin showing stronger interaction than azithromycin and erythromycin. Azithromycin 260-272 ATP binding cassette subfamily B member 1 Homo sapiens 167-171 20231397-8 2010 Additionally, azithromycin increased the number of CD11b(+) monocytes and CD4(+) T cells that infiltrated the alveolar compartment. Azithromycin 14-26 integrin subunit alpha M Homo sapiens 51-56 20621639-1 2010 In this study five macrolide antibiotics (azithromycin, erythromycin, clarithromycin, roxithromycin and telithromycin) were compared based on their ability to interact with human MDR1 (ABCB1, P-glycoprotein), studied from two main aspects: by determining the influence of macrolide antibiotics on MDR1 function, as well as the influence of MDR1 on macrolide accumulation in MES-SA/Dx5 cells overexpressing human MDR1. Azithromycin 42-54 ATP binding cassette subfamily B member 1 Homo sapiens 179-183 20621639-1 2010 In this study five macrolide antibiotics (azithromycin, erythromycin, clarithromycin, roxithromycin and telithromycin) were compared based on their ability to interact with human MDR1 (ABCB1, P-glycoprotein), studied from two main aspects: by determining the influence of macrolide antibiotics on MDR1 function, as well as the influence of MDR1 on macrolide accumulation in MES-SA/Dx5 cells overexpressing human MDR1. Azithromycin 42-54 ATP binding cassette subfamily B member 1 Homo sapiens 185-190 20570573-9 2010 Upon further analysis, PA-infected patients who were treated with azithromycin had the highest arginase activity and the highest number of macrophages that were MR+TLR4-, and both of these markers were inversely related to the FEV(1). Azithromycin 66-78 mannose receptor C-type 1 Homo sapiens 161-163 20570573-9 2010 Upon further analysis, PA-infected patients who were treated with azithromycin had the highest arginase activity and the highest number of macrophages that were MR+TLR4-, and both of these markers were inversely related to the FEV(1). Azithromycin 66-78 toll like receptor 4 Homo sapiens 164-168 20128647-1 2010 Growing data suggest that the antibiotic azithromycin mediates anti-inflammatory activity through the inhibition of the transcription factor NF-kappaB. Azithromycin 41-53 nuclear factor kappa B subunit 1 Homo sapiens 141-150 19893639-0 2009 Azithromycin suppresses interleukin-12p40 expression in lipopolysaccharide and interferon-gamma stimulated macrophages. Azithromycin 0-12 interferon gamma Mus musculus 79-95 19244203-11 2009 Azithromycin, added to cell cultures at 1 mg/liter, significantly reduced proinflammatory cytokine expression (IL-1beta, CCL-2, TNF-alpha) in M1-induced CF and wild-type alveolar macrophages. Azithromycin 0-12 interleukin 1 beta Mus musculus 111-119 19244203-11 2009 Azithromycin, added to cell cultures at 1 mg/liter, significantly reduced proinflammatory cytokine expression (IL-1beta, CCL-2, TNF-alpha) in M1-induced CF and wild-type alveolar macrophages. Azithromycin 0-12 chemokine (C-C motif) ligand 2 Mus musculus 121-126 19244203-11 2009 Azithromycin, added to cell cultures at 1 mg/liter, significantly reduced proinflammatory cytokine expression (IL-1beta, CCL-2, TNF-alpha) in M1-induced CF and wild-type alveolar macrophages. Azithromycin 0-12 tumor necrosis factor Mus musculus 128-137 19893639-13 2009 In conclusion, AZM reduced IL-12p40 transcriptional activity by inhibiting the binding of AP-1, NFAT, and ICSBP to the promoter site. Azithromycin 15-18 interleukin 12b Mus musculus 27-35 19893639-4 2009 We investigated the effect of azithromycin on IL-12p40 production in macrophages after lipopolysaccharide (LPS)/interferon (IFN)-gamma stimulation. Azithromycin 30-42 interleukin 12b Mus musculus 46-54 19893639-9 2009 AZM reduced the induction of IL-12p40 by LPS/IFN-gamma in a dose dependent manner. Azithromycin 0-3 interleukin 12b Mus musculus 29-37 19893639-13 2009 In conclusion, AZM reduced IL-12p40 transcriptional activity by inhibiting the binding of AP-1, NFAT, and ICSBP to the promoter site. Azithromycin 15-18 interferon regulatory factor 8 Mus musculus 106-111 19893639-9 2009 AZM reduced the induction of IL-12p40 by LPS/IFN-gamma in a dose dependent manner. Azithromycin 0-3 interferon gamma Mus musculus 45-54 19893639-10 2009 AZM inhibited the binding of AP-1, nuclear factor of activated T cells (NFAT), and ICSBP, to the DNA binding site in the IL-12p40 promoter. Azithromycin 0-3 interferon regulatory factor 8 Mus musculus 83-88 19893639-10 2009 AZM inhibited the binding of AP-1, nuclear factor of activated T cells (NFAT), and ICSBP, to the DNA binding site in the IL-12p40 promoter. Azithromycin 0-3 interleukin 12b Mus musculus 121-129 19893639-11 2009 AZM also reduced LPS/IFN-gamma-induced IL-12p40 promoter activity. Azithromycin 0-3 interferon gamma Mus musculus 21-30 19893639-11 2009 AZM also reduced LPS/IFN-gamma-induced IL-12p40 promoter activity. Azithromycin 0-3 interleukin 12b Mus musculus 39-47 19893639-12 2009 Phosphorylation of JunB and ICSBP was inhibited by azithromycin-treatment in stimulated cells. Azithromycin 51-63 jun B proto-oncogene Mus musculus 19-23 19893639-12 2009 Phosphorylation of JunB and ICSBP was inhibited by azithromycin-treatment in stimulated cells. Azithromycin 51-63 interferon regulatory factor 8 Mus musculus 28-33 19097986-4 2009 AZM exposure significantly decreased GSTT1 and GSTM1 mRNA and protein expression in IB3-1, restoring the levels to those observed in non-CF C38 cells, which also express lower levels of gamma-glutamyltransferase (GGT) activity than IB3-1. Azithromycin 0-3 glutathione S-transferase theta 1 Homo sapiens 37-42 19633061-0 2009 Azithromycin and clarithromycin inhibit lipopolysaccharide-induced murine pulmonary neutrophilia mainly through effects on macrophage-derived granulocyte-macrophage colony-stimulating factor and interleukin-1beta. Azithromycin 0-12 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 142-190 19633061-0 2009 Azithromycin and clarithromycin inhibit lipopolysaccharide-induced murine pulmonary neutrophilia mainly through effects on macrophage-derived granulocyte-macrophage colony-stimulating factor and interleukin-1beta. Azithromycin 0-12 interleukin 1 beta Mus musculus 195-212 19633061-5 2009 Azithromycin and clarithromycin pretreatment reduced total cell and neutrophil numbers in bronchoalveolar lavage fluid and myeloperoxidase concentration in lung tissue. Azithromycin 0-12 myeloperoxidase Mus musculus 123-138 19788749-9 2009 IL-8 release in TNF-alpha stimulated hu-BEC decreased by 16 +/- 8% (p < 0.05) with AZM (1.5 mg/l). Azithromycin 86-89 C-X-C motif chemokine ligand 8 Homo sapiens 0-4 19788749-9 2009 IL-8 release in TNF-alpha stimulated hu-BEC decreased by 16 +/- 8% (p < 0.05) with AZM (1.5 mg/l). Azithromycin 86-89 tumor necrosis factor Homo sapiens 16-25 19904007-0 2009 Influence of ABCB1 gene polymorphisms on the pharmacokinetics of azithromycin among healthy Chinese Han ethnic subjects. Azithromycin 65-77 ATP binding cassette subfamily B member 1 Homo sapiens 13-18 19904007-1 2009 The aim of this study was to evaluate the effects of ABCB1 gene polymorphisms on azithromycin pharmacokinetics in Chinese Han ethnic subjects. Azithromycin 81-93 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 19904007-8 2009 Our results showed for the first time that azithromycin pharmacokinetics may be influenced by particular polymorphisms of the ABCB1 gene. Azithromycin 43-55 ATP binding cassette subfamily B member 1 Homo sapiens 126-131 19097986-4 2009 AZM exposure significantly decreased GSTT1 and GSTM1 mRNA and protein expression in IB3-1, restoring the levels to those observed in non-CF C38 cells, which also express lower levels of gamma-glutamyltransferase (GGT) activity than IB3-1. Azithromycin 0-3 glutathione S-transferase mu 1 Homo sapiens 47-52 19097986-5 2009 In another CF cell line, 2CFSMEo-, AZM produced 45% reduction in GSTT1 and GSTM1 mRNA levels. Azithromycin 35-38 glutathione S-transferase theta 1 Homo sapiens 65-70 19097986-5 2009 In another CF cell line, 2CFSMEo-, AZM produced 45% reduction in GSTT1 and GSTM1 mRNA levels. Azithromycin 35-38 glutathione S-transferase mu 1 Homo sapiens 75-80 19097986-8 2009 The anti-inflammatory cytokine IL-10 down-modulated GST activity at similar levels, supporting a link between GST inhibition and anti-inflammatory properties of AZM. Azithromycin 161-164 interleukin 10 Homo sapiens 31-36 19622457-0 2009 Azithromycin reduces tumor necrosis factor-alpha production in lipopolysaccharide-stimulated THP-1 monocytic cells by modification of stress response and p38 MAPK pathway. Azithromycin 0-12 mitogen-activated protein kinase 14 Homo sapiens 154-157 19429717-8 2009 RESULTS: Compared to treatment with PBS solution, azithromycin attenuated the ovalbumin-dependent airway inflammation. Azithromycin 50-62 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 78-87 19429717-10 2009 In addition, azithromycin attenuated the expression of cytokines (eg, interleukin [IL]-13 and IL-5) and chemokines (eg, CCL2, CCL3, and CCL4) in the BAL fluid and abrogated the extent of mucous cell metaplasia. Azithromycin 13-25 interleukin 5 Mus musculus 94-98 19429717-10 2009 In addition, azithromycin attenuated the expression of cytokines (eg, interleukin [IL]-13 and IL-5) and chemokines (eg, CCL2, CCL3, and CCL4) in the BAL fluid and abrogated the extent of mucous cell metaplasia. Azithromycin 13-25 chemokine (C-C motif) ligand 2 Mus musculus 120-124 19429717-10 2009 In addition, azithromycin attenuated the expression of cytokines (eg, interleukin [IL]-13 and IL-5) and chemokines (eg, CCL2, CCL3, and CCL4) in the BAL fluid and abrogated the extent of mucous cell metaplasia. Azithromycin 13-25 chemokine (C-C motif) ligand 3 Mus musculus 126-130 19429717-10 2009 In addition, azithromycin attenuated the expression of cytokines (eg, interleukin [IL]-13 and IL-5) and chemokines (eg, CCL2, CCL3, and CCL4) in the BAL fluid and abrogated the extent of mucous cell metaplasia. Azithromycin 13-25 chemokine (C-C motif) ligand 4 Mus musculus 136-140 19429717-11 2009 Similar antiinflammatory effects were observed when azithromycin treatment was initiated after the ovalbumin challenge. Azithromycin 52-64 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 99-108 19271151-5 2009 AZM administration was associated with significant reductions in bacterial load, decreased lung inflammation, and increased levels of IFN-gamma. Azithromycin 0-3 interferon gamma Mus musculus 134-143 19622457-2 2009 We investigated in vitro the effect of azithromycin on tumor necrosis factor alpha (TNF-alpha) production in lipopolysaccharide (LPS)-stimulated THP-1 cells, a human monocytic cell line, and compared the results with those for other macrolides, minocycline and ofloxacin. Azithromycin 39-51 tumor necrosis factor Homo sapiens 84-93 19622457-3 2009 In the presence of LPS, treatment with azithromycin (AZM) resulted in a significant decrease in LPS-induced TNF-alpha production compared to that with other antimicrobial agents. Azithromycin 39-51 tumor necrosis factor Homo sapiens 108-117 19622457-3 2009 In the presence of LPS, treatment with azithromycin (AZM) resulted in a significant decrease in LPS-induced TNF-alpha production compared to that with other antimicrobial agents. Azithromycin 53-56 tumor necrosis factor Homo sapiens 108-117 19622457-4 2009 the results of phosphorylation of three MAPKs, ERK, JNK and p38, indicated that the phospho-p38 level was reduced by AZM. Azithromycin 117-120 mitogen-activated protein kinase 14 Homo sapiens 60-63 19622457-4 2009 the results of phosphorylation of three MAPKs, ERK, JNK and p38, indicated that the phospho-p38 level was reduced by AZM. Azithromycin 117-120 mitogen-activated protein kinase 14 Homo sapiens 92-95 19622457-7 2009 Interestingly, the induction of HSP-70 by LPS was attenuated with the concurrent addition of AZM in the cells. Azithromycin 93-96 heat shock protein family A (Hsp70) member 4 Homo sapiens 32-38 19622457-8 2009 AZM was found to restrain TNF-alpha production by monocytes at least in part by modifying the HSp-70 and p38 related signaling pathways to LPS stimulation. Azithromycin 0-3 tumor necrosis factor Homo sapiens 26-35 19622457-8 2009 AZM was found to restrain TNF-alpha production by monocytes at least in part by modifying the HSp-70 and p38 related signaling pathways to LPS stimulation. Azithromycin 0-3 heat shock protein family A (Hsp70) member 4 Homo sapiens 94-100 19622457-8 2009 AZM was found to restrain TNF-alpha production by monocytes at least in part by modifying the HSp-70 and p38 related signaling pathways to LPS stimulation. Azithromycin 0-3 mitogen-activated protein kinase 14 Homo sapiens 105-108 19661014-0 2009 Macrolide antibiotics like azithromycin increase lipopolysaccharide-induced IL-8 production by human gingival fibroblasts. Azithromycin 27-39 C-X-C motif chemokine ligand 8 Homo sapiens 76-80 19661014-7 2009 AZM increased PgLPS-induced IL-8 production dose-dependently, while AZM did not alter IL-6 and PGE2 productions. Azithromycin 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 28-32 19052724-17 2009 At lower concentrations (600 mg/L) azithromycin provokes a stronger upregulation of the proinflammatory antigens: CD34 (+17%), E-selectin (+18%), ICAM-1 (+27%) and VCAM-1 (+17%). Azithromycin 35-47 CD34 molecule Homo sapiens 114-118 19661014-11 2009 However, the use of the inhibitors of cell signaling pathway failed to reveal the mechanism that AZM enhanced PgLPS-induced IL-8 production. Azithromycin 97-100 C-X-C motif chemokine ligand 8 Homo sapiens 124-128 19661014-13 2009 Because AZM increased LPS-induced IL-8 production by HGFs, the possibility is considered that neutrophils may be migrated to periodontal tissue and phagocytize the periodontopathic bacteria more efficiently. Azithromycin 8-11 C-X-C motif chemokine ligand 8 Homo sapiens 34-38 19503797-8 2009 AZT pretreatment prevented the up-regulation of some genes, such as MUC5AC and MMP9, triggered by the inflammatory stimulus, but the up-regulation of other inflammatory genes, e.g., cytokines and chemokines, such as interleukin-8, was not affected. Azithromycin 0-3 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 68-74 19503797-8 2009 AZT pretreatment prevented the up-regulation of some genes, such as MUC5AC and MMP9, triggered by the inflammatory stimulus, but the up-regulation of other inflammatory genes, e.g., cytokines and chemokines, such as interleukin-8, was not affected. Azithromycin 0-3 matrix metallopeptidase 9 Homo sapiens 79-83 19503797-8 2009 AZT pretreatment prevented the up-regulation of some genes, such as MUC5AC and MMP9, triggered by the inflammatory stimulus, but the up-regulation of other inflammatory genes, e.g., cytokines and chemokines, such as interleukin-8, was not affected. Azithromycin 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 216-229 19503797-10 2009 Notably, secreted IL-8 protein levels did not reflect mRNA levels, and were, in fact, higher after AZT pretreatment in cultures exposed to the inflammatory stimulus, suggesting that AZT can affect inflammatory pathways other than by altering gene expression. Azithromycin 99-102 C-X-C motif chemokine ligand 8 Homo sapiens 18-22 19503797-10 2009 Notably, secreted IL-8 protein levels did not reflect mRNA levels, and were, in fact, higher after AZT pretreatment in cultures exposed to the inflammatory stimulus, suggesting that AZT can affect inflammatory pathways other than by altering gene expression. Azithromycin 182-185 C-X-C motif chemokine ligand 8 Homo sapiens 18-22 19357159-3 2009 Azithromycin-resistant strains (MIC > or = 1 mg/L) were genetically analysed by N. gonorrhoeae multi-antigen sequence typing (NG-MAST) and PFGE. Azithromycin 0-12 sulfatase modifying factor 2 Homo sapiens 142-146 19508161-7 2009 Azithromycin-treated mice did not eliminate C. pneumoniae from lungs by 3 weeks after inoculation but had significantly lower loads (42 genomes per 100 mg) than did control mice (219 genomes per 100 mg) or anti-TNF-alpha antibody-treated mice (3090 genomes per 100 mg). Azithromycin 0-12 tumor necrosis factor Mus musculus 211-220 19052724-17 2009 At lower concentrations (600 mg/L) azithromycin provokes a stronger upregulation of the proinflammatory antigens: CD34 (+17%), E-selectin (+18%), ICAM-1 (+27%) and VCAM-1 (+17%). Azithromycin 35-47 selectin E Homo sapiens 127-137 19052724-17 2009 At lower concentrations (600 mg/L) azithromycin provokes a stronger upregulation of the proinflammatory antigens: CD34 (+17%), E-selectin (+18%), ICAM-1 (+27%) and VCAM-1 (+17%). Azithromycin 35-47 intercellular adhesion molecule 1 Homo sapiens 146-152 19052724-17 2009 At lower concentrations (600 mg/L) azithromycin provokes a stronger upregulation of the proinflammatory antigens: CD34 (+17%), E-selectin (+18%), ICAM-1 (+27%) and VCAM-1 (+17%). Azithromycin 35-47 vascular cell adhesion molecule 1 Homo sapiens 164-170 19131424-10 2009 When the complete orf2 was cloned, it conferred high-level resistance to erythromycin and azithromycin, and the resistance property could be partially inhibited using the efflux inhibitor Phe-Arg beta-naphthylamide dihydrochloride. Azithromycin 90-102 hypothetical protein Escherichia coli 18-22 19345617-6 2009 In contrast, in CF cells, azithromycin increased KC and TNF-alpha expression under non-stimulated and LPS-stimulated conditions, respectively. Azithromycin 26-38 tumor necrosis factor Mus musculus 56-65 19337904-8 2009 A CFTR inhibitor significantly reduced AZM-stimulated Cl- efflux from CFBE cells. Azithromycin 39-42 CF transmembrane conductance regulator Homo sapiens 2-6 18946018-5 2008 In cyclosporine A-treated renal transplant fibroblasts, azithromycin blocked the accumulation of total collagen in culture media and the increase in type I collagen mRNA level, but recovered the reduced MMP-2 mRNA level to the control. Azithromycin 56-68 matrix metallopeptidase 2 Homo sapiens 203-208 18946018-4 2008 Azithromycin elevated the reduced metalloproteinase (MMP)-1 and MMP-2 activities in cyclosporine A-treated renal transplant fibroblasts and normal fibroblasts. Azithromycin 0-12 matrix metallopeptidase 1 Homo sapiens 34-59 19224644-7 2009 RESULTS: For a majority of Zip Codes the relative standard errors (RSEs) of rates calculated prior to AZM were greater than 20%. Azithromycin 102-105 death associated protein kinase 3 Homo sapiens 27-30 18853090-8 2009 CONCLUSIONS: Azithromycin does not improve late angiographic outcomes but attenuates the elevation of C-reactive protein levels after stenting, indicating an anti-inflammatory effect. Azithromycin 13-25 C-reactive protein Homo sapiens 102-120 18931390-7 2009 Azithromycin and clarithromycin had inhibitory effects on overproduction of MUC5AC induced by HNP-1 or LPS stimulation. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 76-82 18931390-9 2009 Phosphorylation of ERK1/2 was induced by HNP-1 or LPS stimulation, and azithromycin, clarithromycin and telithromycin had inhibitory effects on ERK1/2 phosphorylation induced by LPS, but not by HNP-1. Azithromycin 71-83 mitogen-activated protein kinase 3 Homo sapiens 19-25 18931390-9 2009 Phosphorylation of ERK1/2 was induced by HNP-1 or LPS stimulation, and azithromycin, clarithromycin and telithromycin had inhibitory effects on ERK1/2 phosphorylation induced by LPS, but not by HNP-1. Azithromycin 71-83 mitogen-activated protein kinase 3 Homo sapiens 144-150 18946018-4 2008 Azithromycin elevated the reduced metalloproteinase (MMP)-1 and MMP-2 activities in cyclosporine A-treated renal transplant fibroblasts and normal fibroblasts. Azithromycin 0-12 matrix metallopeptidase 2 Homo sapiens 64-69 18946018-6 2008 These results suggest that azithromycin may improve CIGO by blocking cyclosporine A-induced cell proliferation and collagen synthesis, and by activating MMP-2 in gingival fibroblasts of persons with cyclosporine A-induced gingival overgrowth. Azithromycin 27-39 matrix metallopeptidase 2 Homo sapiens 153-158 18761689-2 2008 Clinical isolates with increased resistance to erythromycin and azithromycin frequently harbour mutations in the mtrR structural gene, which encodes a repressor of the mtrCDE operon, or the mtrR promoter region. Azithromycin 64-76 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Mus musculus 113-117 18971093-9 2008 Azithromycin caused a significant decrease in the LPS-stimulated IL-8 and GM-CSF release. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 65-69 18971093-9 2008 Azithromycin caused a significant decrease in the LPS-stimulated IL-8 and GM-CSF release. Azithromycin 0-12 colony stimulating factor 2 Homo sapiens 74-80 18761689-2 2008 Clinical isolates with increased resistance to erythromycin and azithromycin frequently harbour mutations in the mtrR structural gene, which encodes a repressor of the mtrCDE operon, or the mtrR promoter region. Azithromycin 64-76 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Mus musculus 190-194 18758509-6 2008 The alkalinizing lysosomotropic drugs chloroquine, hydroxychloroquine, amodiaquine, and azithromycin had a similar effect on the overall production of mature bioactive TGFbeta. Azithromycin 88-100 transforming growth factor beta 1 Homo sapiens 168-175 18487355-14 2008 Whereas clarithromycin, azithromycin, and moxifloxacin individually were able to inhibit TNF-alpha-induction of IL-8, each failed to inhibit MMF-induction of IL-8. Azithromycin 24-36 C-X-C motif chemokine ligand 8 Homo sapiens 112-116 18420960-0 2008 Azithromycin improves macrophage phagocytic function and expression of mannose receptor in chronic obstructive pulmonary disease. Azithromycin 0-12 mannose receptor C-type 1 Homo sapiens 71-87 18420960-4 2008 METHODS: In vitro effects of azithromycin on AM expression of MR were investigated. Azithromycin 29-41 mannose receptor C-type 1 Homo sapiens 62-64 18420960-10 2008 In patients with COPD, after azithromycin therapy, we observed significantly improved AM phagocytic ability (pre: 9.9%; post: 15.1%), reduced bronchial epithelial cell apoptosis (pre: 30.0%; post: 19.7%), and increased MR and reduced inflammatory markers in the peripheral blood. Azithromycin 29-41 mannose receptor C-type 1 Homo sapiens 219-221 18420960-11 2008 These findings implicate the MR in the defective phagocytic function of AMs in COPD and as a target for the azithromycin-mediated improvement in phagocytic ability. Azithromycin 108-120 mannose receptor C-type 1 Homo sapiens 29-31 18226504-4 2008 By making such an extrapolation and using pharmacokinetic modelling with conservative assumptions on MIC values against Borrelia burgdorferi, it is hypothesised that a single 500 mg dose of azithromycin in humans should have comparable efficacy to doxycycline for the prevention of Lyme disease. Azithromycin 190-202 microphthalmia Japan Mus musculus 101-104 18435685-8 2008 Leukocytes, lymphocytes, neutrophils, 8-isoprostane and IL-1beta levels after ischaemia and reperfusion were significantly reduced in mice treated with azithromycin. Azithromycin 152-164 interleukin 1 beta Mus musculus 56-64 18503189-4 2008 Deletion of crp significantly increased the resistance of the E. coli strain to oxacillin, azithromycin, erythromycin and crystal violet. Azithromycin 91-103 catabolite gene activator protein Escherichia coli 12-15 19281070-0 2008 Use of azithromycin in the treatment of acute exacerbations of COPD. Azithromycin 7-19 COPD Homo sapiens 63-67 18230686-6 2008 Azithromycin-treated J774 macrophages demonstrated a significantly reduced production of the pro-inflammatory cytokines IL-12 and IL-6, increased production of the anti-inflammatory cytokine IL-10 and decreased the ratio of IL-12 to IL-10 by 60%. Azithromycin 0-12 interleukin 6 Mus musculus 130-134 18230686-6 2008 Azithromycin-treated J774 macrophages demonstrated a significantly reduced production of the pro-inflammatory cytokines IL-12 and IL-6, increased production of the anti-inflammatory cytokine IL-10 and decreased the ratio of IL-12 to IL-10 by 60%. Azithromycin 0-12 interleukin 10 Mus musculus 191-196 18230686-6 2008 Azithromycin-treated J774 macrophages demonstrated a significantly reduced production of the pro-inflammatory cytokines IL-12 and IL-6, increased production of the anti-inflammatory cytokine IL-10 and decreased the ratio of IL-12 to IL-10 by 60%. Azithromycin 0-12 interleukin 10 Mus musculus 233-238 18230686-8 2008 The presence of azithromycin increased arginase (M2 effector molecule) activity 10-fold in cells stimulated with IFNgamma and LPS, and iNOS protein (M1 effector molecule) concentrations were attenuated by the drug. Azithromycin 16-28 interferon gamma Mus musculus 113-121 18230544-0 2007 Effects of azithromycin on the expression of ATP binding cassette transporters in epithelial cells from the airways of cystic fibrosis patients. Azithromycin 11-23 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 45-65 18230544-4 2007 After AZM treatment we found modest differences in MRP1 and MDR1 mRNA expression while protein levels were unaffected. Azithromycin 6-9 ATP binding cassette subfamily B member 1 Homo sapiens 60-64 18230544-5 2007 The ability of AZM to regulate MRP1 promoter transcriptional activity was excluded by gene reporter assays. Azithromycin 15-18 ATP binding cassette subfamily C member 1 Homo sapiens 31-35 18053438-0 2007 Azithromycin for PID beats doxycycline on all counts. Azithromycin 0-12 metastasis associated 1 family member 2 Homo sapiens 17-20 18230544-1 2007 Induction of ATP Binding Cassette (ABC) proteins involved in chloride transport has been proposed as a possible mechanism of the beneficial effects of azithromycin (AZM) in cystic fibrosis (CF) patients. Azithromycin 151-163 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 13-33 18230544-1 2007 Induction of ATP Binding Cassette (ABC) proteins involved in chloride transport has been proposed as a possible mechanism of the beneficial effects of azithromycin (AZM) in cystic fibrosis (CF) patients. Azithromycin 151-163 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 35-38 18230544-1 2007 Induction of ATP Binding Cassette (ABC) proteins involved in chloride transport has been proposed as a possible mechanism of the beneficial effects of azithromycin (AZM) in cystic fibrosis (CF) patients. Azithromycin 165-168 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 13-33 18230544-1 2007 Induction of ATP Binding Cassette (ABC) proteins involved in chloride transport has been proposed as a possible mechanism of the beneficial effects of azithromycin (AZM) in cystic fibrosis (CF) patients. Azithromycin 165-168 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 35-38 18230544-2 2007 This study focused on the effects of AZM on mRNA and protein expression of Multidrug Resistance-associated Protein 1 (MRP1) and Multidrug Resistance Protein 1 (MDR1) by real-time quantitative PCR, flow cytometry and gene reporter assays in two CF and two isogenic non-CF airway epithelial cell lines. Azithromycin 37-40 ATP binding cassette subfamily C member 1 Homo sapiens 75-116 18230544-2 2007 This study focused on the effects of AZM on mRNA and protein expression of Multidrug Resistance-associated Protein 1 (MRP1) and Multidrug Resistance Protein 1 (MDR1) by real-time quantitative PCR, flow cytometry and gene reporter assays in two CF and two isogenic non-CF airway epithelial cell lines. Azithromycin 37-40 ATP binding cassette subfamily C member 1 Homo sapiens 118-122 18230544-2 2007 This study focused on the effects of AZM on mRNA and protein expression of Multidrug Resistance-associated Protein 1 (MRP1) and Multidrug Resistance Protein 1 (MDR1) by real-time quantitative PCR, flow cytometry and gene reporter assays in two CF and two isogenic non-CF airway epithelial cell lines. Azithromycin 37-40 ATP binding cassette subfamily B member 1 Homo sapiens 128-158 18230544-2 2007 This study focused on the effects of AZM on mRNA and protein expression of Multidrug Resistance-associated Protein 1 (MRP1) and Multidrug Resistance Protein 1 (MDR1) by real-time quantitative PCR, flow cytometry and gene reporter assays in two CF and two isogenic non-CF airway epithelial cell lines. Azithromycin 37-40 ATP binding cassette subfamily B member 1 Homo sapiens 160-164 18230544-4 2007 After AZM treatment we found modest differences in MRP1 and MDR1 mRNA expression while protein levels were unaffected. Azithromycin 6-9 ATP binding cassette subfamily C member 1 Homo sapiens 51-55 17667842-3 2007 We studied the effect of azithromycin (AZM) on the suppression of NF-kappaB activation and the synthesis of pro-inflammatory cytokines IL-6 and IL-8 by TA cells obtained from premature infants. Azithromycin 25-37 nuclear factor kappa B subunit 1 Homo sapiens 66-75 17667842-3 2007 We studied the effect of azithromycin (AZM) on the suppression of NF-kappaB activation and the synthesis of pro-inflammatory cytokines IL-6 and IL-8 by TA cells obtained from premature infants. Azithromycin 25-37 C-X-C motif chemokine ligand 8 Homo sapiens 144-148 17667842-3 2007 We studied the effect of azithromycin (AZM) on the suppression of NF-kappaB activation and the synthesis of pro-inflammatory cytokines IL-6 and IL-8 by TA cells obtained from premature infants. Azithromycin 39-42 nuclear factor kappa B subunit 1 Homo sapiens 66-75 17667842-3 2007 We studied the effect of azithromycin (AZM) on the suppression of NF-kappaB activation and the synthesis of pro-inflammatory cytokines IL-6 and IL-8 by TA cells obtained from premature infants. Azithromycin 39-42 C-X-C motif chemokine ligand 8 Homo sapiens 144-148 17667842-6 2007 Stimulation of TA cells by TNF-alpha increased the activation of NF-kappaB, which was suppressed by the addition of AZM. Azithromycin 116-119 tumor necrosis factor Homo sapiens 27-36 17667842-6 2007 Stimulation of TA cells by TNF-alpha increased the activation of NF-kappaB, which was suppressed by the addition of AZM. Azithromycin 116-119 nuclear factor kappa B subunit 1 Homo sapiens 65-74 17667842-8 2007 AZM significantly reduced the IL-6 and IL-8 production to the levels similar to control. Azithromycin 0-3 interleukin 6 Homo sapiens 30-34 17667842-8 2007 AZM significantly reduced the IL-6 and IL-8 production to the levels similar to control. Azithromycin 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 39-43 17667842-9 2007 TNF-alpha stimulation also increased the degradation of IkappaB-alpha, which was restored with the addition of AZM. Azithromycin 111-114 tumor necrosis factor Homo sapiens 0-9 17667842-9 2007 TNF-alpha stimulation also increased the degradation of IkappaB-alpha, which was restored with the addition of AZM. Azithromycin 111-114 NFKB inhibitor alpha Homo sapiens 56-69 17296622-7 2007 These experiments demonstrated that the OATP1B1- and OATP1B3-mediated uptake of BSP and pravastatin can be inhibited by increasing concentrations of all macrolides except azithromycin. Azithromycin 171-183 solute carrier organic anion transporter family member 1B1 Homo sapiens 40-47 17963679-13 2007 Finally, azithromycin-treated pups had lower levels of IL-6 in lung homogenate from the hyperoxia groups (p < .05). Azithromycin 9-21 interleukin 6 Rattus norvegicus 55-59 17963679-14 2007 Azithromycin treatment resulted in improved survival, less emphysematous change, and decreased IL-6 levels in an animal model of BPD. Azithromycin 0-12 interleukin 6 Rattus norvegicus 95-99 17994436-0 2007 Azithromycin prevents recurrence of severe trichiasis following trichiasis surgery: STAR trial. Azithromycin 0-12 steroidogenic acute regulatory protein Homo sapiens 84-88 17296622-7 2007 These experiments demonstrated that the OATP1B1- and OATP1B3-mediated uptake of BSP and pravastatin can be inhibited by increasing concentrations of all macrolides except azithromycin. Azithromycin 171-183 solute carrier organic anion transporter family member 1B3 Homo sapiens 53-60 17210769-0 2007 Azithromycin selectively reduces tumor necrosis factor alpha levels in cystic fibrosis airway epithelial cells. Azithromycin 0-12 tumor necrosis factor Homo sapiens 33-60 17210769-6 2007 In CF cells, AZM treatment causes a 30% reduction of TNF-alpha mRNA levels (P < 0.05) and a 45% decrease in TNF-alpha secretion (P < 0.05), reaching approximately the levels of the untreated isogenic non-CF cells. Azithromycin 13-16 tumor necrosis factor Homo sapiens 53-62 17210769-6 2007 In CF cells, AZM treatment causes a 30% reduction of TNF-alpha mRNA levels (P < 0.05) and a 45% decrease in TNF-alpha secretion (P < 0.05), reaching approximately the levels of the untreated isogenic non-CF cells. Azithromycin 13-16 tumor necrosis factor Homo sapiens 111-120 17210769-10 2007 The results of our study support the anti-inflammatory activities of this macrolide, since we show that AZM reduced the levels of TNF-alpha and propose inhibitions of NF-kappaB and Sp1 DNA binding as possible mechanisms of this effect. Azithromycin 104-107 tumor necrosis factor Homo sapiens 130-139 17306081-9 2007 CONCLUSIONS: Azithromycin may inhibit NF-kappaB activity, decrease TNF-alpha secretion and thus lessen cytotoxicity of CSE to A549 cells. Azithromycin 13-25 tumor necrosis factor Homo sapiens 67-76 17302905-3 2007 A 15-membered macrolide, AZM, and a 14-membered macrolide, CAM, significantly enhanced the intensity of a co-stimulatory molecule, CD80, on DCs but not CD86 and CD40. Azithromycin 25-28 CD80 antigen Mus musculus 131-135 17302905-4 2007 AZM significantly increased the production of IL-10 and CAM significantly inhibited the production of IL-6 by DCs. Azithromycin 0-3 interleukin 10 Mus musculus 46-51 17302905-4 2007 AZM significantly increased the production of IL-10 and CAM significantly inhibited the production of IL-6 by DCs. Azithromycin 0-3 interleukin 6 Mus musculus 102-106 17302905-6 2007 Moreover, AZM increased IL-10 and CAM decreased IL-2 productions significantly, when naive T cells derived from spleen were co-cultured with DCs treated in advance with LPS and these macrolides. Azithromycin 10-13 interleukin 10 Mus musculus 24-29 17302905-6 2007 Moreover, AZM increased IL-10 and CAM decreased IL-2 productions significantly, when naive T cells derived from spleen were co-cultured with DCs treated in advance with LPS and these macrolides. Azithromycin 10-13 interleukin 2 Mus musculus 48-52 17061983-7 2007 IL17-induced IL8 production was decreased by both erythromycin and azithromycin. Azithromycin 67-79 interleukin 17A Homo sapiens 0-4 17110371-11 2007 Molecular modeling of mutant PfRpl4 with AZ suggests an altered orientation of the L75 side chain that could preclude AZ binding. Azithromycin 41-43 RPL4 Plasmodium falciparum 29-35 17110371-12 2007 These data imply that AZ acts on the apicoplast bacterial-like translation machinery and identify Pfrpl4 as a potential marker of resistance. Azithromycin 22-24 RPL4 Plasmodium falciparum 98-104 17012372-14 2007 In conclusion, TNF-alpha and IL-1beta induce an exaggerated inflammatory response in CF airway cells, inhibited by MXF more than by CIP or AZM. Azithromycin 139-142 tumor necrosis factor Homo sapiens 15-24 17012372-14 2007 In conclusion, TNF-alpha and IL-1beta induce an exaggerated inflammatory response in CF airway cells, inhibited by MXF more than by CIP or AZM. Azithromycin 139-142 interleukin 1 beta Homo sapiens 29-37 17061983-7 2007 IL17-induced IL8 production was decreased by both erythromycin and azithromycin. Azithromycin 67-79 C-X-C motif chemokine ligand 8 Homo sapiens 13-16 17061983-8 2007 In nonstimulated condition, IL8 production only increased at the highest dose of azithromycin. Azithromycin 81-93 C-X-C motif chemokine ligand 8 Homo sapiens 28-31 17045242-3 2006 AZM reduced about 40% of IL-8 mRNA and protein expression (n=9, p=0.02, and n=4, p=0.00011) in CF cells reaching the levels of non-CF cells. Azithromycin 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 25-29 17207028-11 2007 Moreover, maximum C-reactive protein values also appeared to be lower in the azithromycin group than in the no-treatment group and the cefcapene group. Azithromycin 77-89 C-reactive protein Homo sapiens 18-36 18027988-4 2007 RESULTS: All macrolides inhibited P-glycoprotein-mediated digoxin transport, with concentrations producing 50% inhibition (IC(50)) values of 1.8, 4.1, 15.4, 21.8 and 22.7 micromol/L for telithromycin, clarithromycin, roxithromycin, azithromycin and erythromycin, respectively. Azithromycin 232-244 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 17045242-4 2006 In the presence of AZM we found about 50% and 70% reduction of NF-kappaB and AP-1 DNA binding, respectively (n=3, p=0.01, and n=3, p=0.0017), leading to levels of non-CF cells. Azithromycin 19-22 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-81 17088870-5 2006 EXPERIMENTAL APPROACH & KEY RESULTS: In transfected HEK cells, the IC(50)s for I (hERG) were 45+/-6 and 856+/-259 microg ml(-1) for moxifloxacin and azithromycin, respectively. Azithromycin 153-165 ETS transcription factor ERG Homo sapiens 86-90 17083011-8 2006 In contrast, there was killing of ingested GAS after exposure of epithelial cells to either erythromycin or azithromycin. Azithromycin 108-120 gastrin Homo sapiens 43-46 16185859-2 2006 We conducted an open-label study of azithromycin (500 mg daily for 2 weeks) in 9 adult CF patients to explore 3 possible mechanisms: up-regulation of the multi-drug resistance (MDR) or cystic fibrosis transmembrane regulator (CFTR) proteins, correction of epithelial ion transport and reduced bacterial adherence. Azithromycin 36-48 CF transmembrane conductance regulator Homo sapiens 185-224 16741151-0 2006 Azithromycin reduces airway neutrophilia and interleukin-8 in patients with bronchiolitis obliterans syndrome. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 45-58 16741151-4 2006 HYPOTHESES: (1) Azithromycin reduces airway neutrophilia and interleukin (IL)-8 and (2) airway neutrophilia predicts the improvement in FEV(1). Azithromycin 16-28 C-X-C motif chemokine ligand 8 Homo sapiens 61-79 16741151-11 2006 CONCLUSION: Azithromycin significantly reduces airway neutrophilia and IL-8 mRNA in patients with BOS. Azithromycin 12-24 C-X-C motif chemokine ligand 8 Homo sapiens 71-75 16698012-4 2006 Our results show that azithromycin (10 and 100 mg/kg) significantly attenuated the intraperitoneal LPS-induced increase in plasma TNF-alpha concentration. Azithromycin 22-34 tumor necrosis factor Mus musculus 130-139 16698012-7 2006 In the same model, azithromycin given intraperitoneally significantly improved inflammatory markers (total cell number, neutrophil percentage and MIP-2 concentration) in bronchoalveolar lavage fluid. Azithromycin 19-31 chemokine (C-X-C motif) ligand 2 Mus musculus 146-151 16641453-5 2006 Immunocytochemistry and Western blotting showed that addition of azithromycin changed the locations of proteins in cell cultures and induced processing of the tight junction proteins claudin-1 and claudin-4, occludin, and junctional adhesion molecule-A. Azithromycin 65-77 claudin 1 Homo sapiens 183-192 16641453-5 2006 Immunocytochemistry and Western blotting showed that addition of azithromycin changed the locations of proteins in cell cultures and induced processing of the tight junction proteins claudin-1 and claudin-4, occludin, and junctional adhesion molecule-A. Azithromycin 65-77 claudin 4 Homo sapiens 197-206 16641453-5 2006 Immunocytochemistry and Western blotting showed that addition of azithromycin changed the locations of proteins in cell cultures and induced processing of the tight junction proteins claudin-1 and claudin-4, occludin, and junctional adhesion molecule-A. Azithromycin 65-77 occludin Homo sapiens 208-216 17064416-8 2006 In cystic fibrosis mice, azithromycin attenuated cellular infiltration in both baseline and induced inflammatory condition, and inhibited cytokine (tumor necrosis factor-alpha and macrophage inflammatory protein-2) release in lipopolysaccharide-induced inflammation. Azithromycin 25-37 tumor necrosis factor Mus musculus 148-175 17064416-8 2006 In cystic fibrosis mice, azithromycin attenuated cellular infiltration in both baseline and induced inflammatory condition, and inhibited cytokine (tumor necrosis factor-alpha and macrophage inflammatory protein-2) release in lipopolysaccharide-induced inflammation. Azithromycin 25-37 chemokine (C-X-C motif) ligand 2 Mus musculus 180-213 16185859-2 2006 We conducted an open-label study of azithromycin (500 mg daily for 2 weeks) in 9 adult CF patients to explore 3 possible mechanisms: up-regulation of the multi-drug resistance (MDR) or cystic fibrosis transmembrane regulator (CFTR) proteins, correction of epithelial ion transport and reduced bacterial adherence. Azithromycin 36-48 CF transmembrane conductance regulator Homo sapiens 226-230 16416302-3 2006 METHODS: The in vitro kinetic constants of CYP3A inactivation (K (I) and k (inact)) were estimated by varying the time of pre-incubation and the concentration of troleandomycin, erythromycin, clarithromycin, roxithromycin or azithromycin. Azithromycin 225-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 16395097-4 2006 Azithromycin-resistant organisms were tested for the presence of mef and erm sequences by polymerase chain reaction. Azithromycin 0-12 E74 like ETS transcription factor 4 Homo sapiens 65-68 16464259-2 2006 MRP1 has been proposed as a potential modifier gene and/or as novel target for pharmacotherapy of CF to explain the clinical benefits observed in some CF patients treated with the macrolide AZM. Azithromycin 190-193 ATP binding cassette subfamily C member 1 Homo sapiens 0-4 16085674-5 2006 AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). Azithromycin 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 19-23 16085674-5 2006 AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). Azithromycin 153-156 C-X-C motif chemokine ligand 8 Homo sapiens 19-23 16085674-5 2006 AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). Azithromycin 153-156 C-X-C motif chemokine ligand 8 Homo sapiens 184-188 16085674-5 2006 AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). Azithromycin 153-156 C-X-C motif chemokine ligand 8 Homo sapiens 184-188 16395097-8 2006 All mef/erm-positive organisms demonstrated azithromycin minimum inhibitory concentrations > or =256 microg/mL and were coresistant to all other agents tested. Azithromycin 44-56 E74 like ETS transcription factor 4 Homo sapiens 4-7 16113783-4 2005 The aim of this study was to determine the effect of an immunosuppressant macrolide, rapamycin (Sirolimus), on the expression of TF and its inhibitor (TFPI) by monocytic cells (human blood mononuclear and THP-1 cells) and human aortic smooth muscle cells, in comparison with FK-506 and azithromycin. Azithromycin 286-298 coagulation factor III, tissue factor Homo sapiens 129-131 16096858-0 2005 Autoantibodies against bactericidal/permeability-increasing protein (BPI-ANCA) in cystic fibrosis patients treated with azithromycin. Azithromycin 120-132 bactericidal permeability increasing protein Homo sapiens 69-72 16096858-3 2005 Our aim was to evaluate whether azithromycin (AZM), through its antiinflammatory effect, could affect the level of BPI-ANCA in CF patients. Azithromycin 32-44 bactericidal permeability increasing protein Homo sapiens 115-118 16096858-3 2005 Our aim was to evaluate whether azithromycin (AZM), through its antiinflammatory effect, could affect the level of BPI-ANCA in CF patients. Azithromycin 46-49 bactericidal permeability increasing protein Homo sapiens 115-118 16167518-8 2005 A significant direct correlation was found between MRP mRNA expression levels and NPD chloride response after azithromycin treatment (p = 0.04, r = 0.78). Azithromycin 110-122 ATP binding cassette subfamily C member 3 Homo sapiens 51-54 16167518-9 2005 In conclusion, azithromycin may induce MRP overexpression and restore chloride conductance in the airways of cystic fibrosis patients. Azithromycin 15-27 ATP binding cassette subfamily C member 3 Homo sapiens 39-42 16113783-4 2005 The aim of this study was to determine the effect of an immunosuppressant macrolide, rapamycin (Sirolimus), on the expression of TF and its inhibitor (TFPI) by monocytic cells (human blood mononuclear and THP-1 cells) and human aortic smooth muscle cells, in comparison with FK-506 and azithromycin. Azithromycin 286-298 tissue factor pathway inhibitor Homo sapiens 151-155 15610401-6 2005 Although a trend towards increased stimulated IL-10 responses with azithromycin was observed, no statistically significant difference was found. Azithromycin 67-79 interleukin 10 Homo sapiens 46-51 15885263-8 2005 Administration of either azithromycin or erythromycin at different dosage (10, 20 and 40 mg/kg orally, daily for 5 consecutive days) significantly (P < 0.05) reduced the colonic damage, MPO and NOS activities as well as TNFalpha level. Azithromycin 25-37 myeloperoxidase Rattus norvegicus 189-192 15885263-8 2005 Administration of either azithromycin or erythromycin at different dosage (10, 20 and 40 mg/kg orally, daily for 5 consecutive days) significantly (P < 0.05) reduced the colonic damage, MPO and NOS activities as well as TNFalpha level. Azithromycin 25-37 tumor necrosis factor Rattus norvegicus 223-231 16400877-9 2005 The 1100 MRSA isolates distributed to four antibiotic resistance patterns on the basis of their resistance to oxacillin, penicillin, amoxicillin+clavulanic acid, azithromycin, clindamycin, amikacin, gentamicin, ciprofloxacin, trimethoprim+sulphamethoxasole, vancomycin and teicoplanin. Azithromycin 162-174 solute carrier family 9 member A6 Homo sapiens 9-13 15325428-3 2004 Lymphocytes treated with clarithromycin, azithromycin and josamycin at a final concentration of 200 microg/ml showed positive staining for Annexin V, Fas and Fas ligand using flow cytometry with time at 12-72 h, while other antibiotics did not. Azithromycin 41-53 annexin A5 Homo sapiens 139-148 15361366-5 2004 This effect was associated with significant decreases in lung levels of tumor necrosis factor-alpha and keratinocyte-derived chemokine in azithromycin-treated mice compared with untreated mice. Azithromycin 138-150 tumor necrosis factor Mus musculus 72-99 15361366-7 2004 Inhibition of chemotaxis correlated with azithromycin-mediated inhibition of extracellular signal-regulated kinase-1 and -2 activation. Azithromycin 41-53 mitogen-activated protein kinase 3 Mus musculus 77-123 15361366-8 2004 This study indicates that the azithromycin treatment in vivo results in significant reduction in airway-specific inflammation, which occurs in part by inhibition of neutrophil recruitment to the lung through reduction in proinflammatory cytokine expression and inhibition of neutrophil migration via the extracellular signal-regulated kinase-1 and -2 signal transduction pathway. Azithromycin 30-42 mitogen-activated protein kinase 3 Mus musculus 304-350 15566918-3 2004 The changes in CFVR were negatively correlated with changes in high-sensitivity C-reactive protein levels in patients receiving azithromycin. Azithromycin 128-140 C-reactive protein Homo sapiens 80-98 15328111-0 2004 Azithromycin inhibits MUC5AC production induced by the Pseudomonas aeruginosa autoinducer N-(3-Oxododecanoyl) homoserine lactone in NCI-H292 Cells. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 22-28 15328111-7 2004 A 15-membered macrolide, azithromycin, inhibited MUC5AC production that was activated by 3O-C(12)-HSL. Azithromycin 25-37 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 49-55 15328111-7 2004 A 15-membered macrolide, azithromycin, inhibited MUC5AC production that was activated by 3O-C(12)-HSL. Azithromycin 25-37 lipase E, hormone sensitive type Homo sapiens 98-101 15328111-8 2004 3O-C(12)-HSL induced extracellular signal-regulated kinase (ERK) 1/2 and I-kappa B phosphorylation in cells, and this induction was suppressed by azithromycin. Azithromycin 146-158 lipase E, hormone sensitive type Homo sapiens 9-12 15251115-0 2004 Clarithromycin and azithromycin induce apoptosis of activated lymphocytes via down-regulation of Bcl-xL. Azithromycin 19-31 BCL2 like 1 Homo sapiens 97-103 15251115-4 2004 CLR and AZM inhibited the expression of Bcl-xL compared with that of control. Azithromycin 8-11 BCL2 like 1 Homo sapiens 40-46 15251115-5 2004 Our results suggest that CLR and AZM enhance apoptosis of activated lymphocytes by down-regulation of Bcl-xL. Azithromycin 33-36 BCL2 like 1 Homo sapiens 102-108 15325428-3 2004 Lymphocytes treated with clarithromycin, azithromycin and josamycin at a final concentration of 200 microg/ml showed positive staining for Annexin V, Fas and Fas ligand using flow cytometry with time at 12-72 h, while other antibiotics did not. Azithromycin 41-53 Fas ligand Homo sapiens 158-168 15524029-1 2004 This paper presents the efficacy and cost of therapy with azithromycin for the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease (COPD). Azithromycin 58-70 COPD Homo sapiens 167-171 15336223-5 2004 Prophylaxis with azithromycin or clarithromycin is recommended for all patients with CD4 counts less than 50 cells/mL. Azithromycin 17-29 CD4 molecule Homo sapiens 85-88 15163653-4 2004 Neutrophils were attracted in vitro to persistently infected HEC-1B cells that had been exposed to penicillin and azithromycin. Azithromycin 114-126 NDC80 kinetochore complex component Homo sapiens 61-66 15252403-8 2004 Incubation with 0.016 microg/mL azithromycin decreased IL-6 levels to a mean of 1516 +/- 402 pg/mL, and incubation with 0.125 and 1 microg/mL azithromycin decreased IL-6 to 871 +/- 364 and 752 +/- 403 pg/mL, respectively. Azithromycin 32-44 interleukin 6 Homo sapiens 55-59 15252403-8 2004 Incubation with 0.016 microg/mL azithromycin decreased IL-6 levels to a mean of 1516 +/- 402 pg/mL, and incubation with 0.125 and 1 microg/mL azithromycin decreased IL-6 to 871 +/- 364 and 752 +/- 403 pg/mL, respectively. Azithromycin 32-44 interleukin 6 Homo sapiens 165-169 15252403-10 2004 The interaction of C pneumoniae with azithromycin treatment was significant, indicating an inhibitory effect of azithromycin on C pneumoniae-induced IL-6 production. Azithromycin 37-49 interleukin 6 Homo sapiens 149-153 15252403-10 2004 The interaction of C pneumoniae with azithromycin treatment was significant, indicating an inhibitory effect of azithromycin on C pneumoniae-induced IL-6 production. Azithromycin 112-124 interleukin 6 Homo sapiens 149-153 15252403-16 2004 Azithromycin reduces C pneumoniae-induced IL-6 production, but not fibrinogen production, by human hepatocytes. Azithromycin 0-12 interleukin 6 Homo sapiens 42-46 14744620-1 2004 The present study aims to investigate whether azithromycin reverses P-glycoprotein-dependent anticancer drug resistance in vitro and modifies the hepatobiliary excretion of doxorubicin, a substrate for P-glycoprotein in vivo. Azithromycin 46-58 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 68-82 14551160-7 2004 On the other hand, pretreatment of TNF-alpha-stimulated A549 cells by erythromycin, clarithromycin, azithromycin, or dexamethasone, but not josamycin, decreased the neutrophil survival-enhancing effects in a dose-dependent manner. Azithromycin 100-112 tumor necrosis factor Homo sapiens 35-44 14551160-9 2004 Erythromycin, clarithromycin, azithromycin, and dexamethasone inhibited TNF-alpha-induced GM-CSF expression in A549 cells at both the protein and messenger RNA levels. Azithromycin 30-42 tumor necrosis factor Homo sapiens 72-81 14551160-9 2004 Erythromycin, clarithromycin, azithromycin, and dexamethasone inhibited TNF-alpha-induced GM-CSF expression in A549 cells at both the protein and messenger RNA levels. Azithromycin 30-42 colony stimulating factor 2 Homo sapiens 90-96 14982769-0 2004 Possible involvement of the drug transporters P glycoprotein and multidrug resistance-associated protein Mrp2 in disposition of azithromycin. Azithromycin 128-140 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 46-60 14982769-0 2004 Possible involvement of the drug transporters P glycoprotein and multidrug resistance-associated protein Mrp2 in disposition of azithromycin. Azithromycin 128-140 ATP binding cassette subfamily C member 2 Rattus norvegicus 105-109 14982769-2 2004 The present study seeks to clarify the contribution of P glycoprotein and/or Mrp2 to the disposition of azithromycin in rats. Azithromycin 104-116 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 55-69 14982769-2 2004 The present study seeks to clarify the contribution of P glycoprotein and/or Mrp2 to the disposition of azithromycin in rats. Azithromycin 104-116 ATP binding cassette subfamily C member 2 Rattus norvegicus 77-81 14982769-4 2004 When rats received an infusion of azithromycin, cyclosporine and probenecid, a validated Mrp2 inhibitor, significantly decreased the steady-state biliary clearance of azithromycin to 5 and 40% of the corresponding control values, respectively. Azithromycin 34-46 ATP binding cassette subfamily C member 2 Rattus norvegicus 89-93 14982769-4 2004 When rats received an infusion of azithromycin, cyclosporine and probenecid, a validated Mrp2 inhibitor, significantly decreased the steady-state biliary clearance of azithromycin to 5 and 40% of the corresponding control values, respectively. Azithromycin 167-179 ATP binding cassette subfamily C member 2 Rattus norvegicus 89-93 14982769-7 2004 Significant reduction in the biliary excretion of azithromycin was observed in Eisai hyperbilirubinemic rats, which have a hereditary deficiency in Mrp2. Azithromycin 50-62 ATP binding cassette subfamily C member 2 Rattus norvegicus 148-152 14982769-9 2004 These results suggest that azithromycin is a substrate for both P glycoprotein and Mrp2 and that the biliary and intestinal excretion of azithromycin is mediated via these two drug transporters. Azithromycin 27-39 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 64-78 14982769-9 2004 These results suggest that azithromycin is a substrate for both P glycoprotein and Mrp2 and that the biliary and intestinal excretion of azithromycin is mediated via these two drug transporters. Azithromycin 27-39 ATP binding cassette subfamily C member 2 Rattus norvegicus 83-87 14744620-1 2004 The present study aims to investigate whether azithromycin reverses P-glycoprotein-dependent anticancer drug resistance in vitro and modifies the hepatobiliary excretion of doxorubicin, a substrate for P-glycoprotein in vivo. Azithromycin 46-58 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 202-216 14744620-7 2004 The present findings suggest that azithromycin overcomes P-glycoprotein-dependent anticancer drug resistance of tumors by inhibiting the binding of doxorubicin to P-glycoprotein in K562/ADR cells and inhibits the hepatobiliary excretion of drugs that are substrates for P-glycoprotein and Mrp2. Azithromycin 34-46 ATP binding cassette subfamily B member 1 Homo sapiens 57-71 14744620-7 2004 The present findings suggest that azithromycin overcomes P-glycoprotein-dependent anticancer drug resistance of tumors by inhibiting the binding of doxorubicin to P-glycoprotein in K562/ADR cells and inhibits the hepatobiliary excretion of drugs that are substrates for P-glycoprotein and Mrp2. Azithromycin 34-46 ATP binding cassette subfamily B member 1 Homo sapiens 163-177 14744620-7 2004 The present findings suggest that azithromycin overcomes P-glycoprotein-dependent anticancer drug resistance of tumors by inhibiting the binding of doxorubicin to P-glycoprotein in K562/ADR cells and inhibits the hepatobiliary excretion of drugs that are substrates for P-glycoprotein and Mrp2. Azithromycin 34-46 ATP binding cassette subfamily B member 1 Homo sapiens 163-177 12742010-3 2003 The effects of azithromycin on CSA disposition kinetics were evaluated in eight stable renal transplant patients. Azithromycin 15-27 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 31-34 14744620-7 2004 The present findings suggest that azithromycin overcomes P-glycoprotein-dependent anticancer drug resistance of tumors by inhibiting the binding of doxorubicin to P-glycoprotein in K562/ADR cells and inhibits the hepatobiliary excretion of drugs that are substrates for P-glycoprotein and Mrp2. Azithromycin 34-46 ATP binding cassette subfamily C member 2 Homo sapiens 289-293 12712826-8 2003 Taking into account the duration of hospitalization, it was shown that the mean total costs of treatment of COPD exacerbation with azithromycin was significantly lower than that of treatment with cefoperazone (2375.9 PLN and 1663.7 PLN, respectively) (p < 0.05). Azithromycin 131-143 phospholamban Homo sapiens 217-220 12623273-5 2003 When azithromycin was added to infected cultures of FSC at 0 or 48 h after infection, the level of IL-6 production was very low. Azithromycin 5-17 interleukin 6 Homo sapiens 99-103 15002174-3 2003 The direct modulating effect of ZF in a concentration of 50 mcg/ml corresponding to the single therapeutic dose of 500 mg/70 kg body weight on the neutrophil oxidase activity evident from increased production of active oxygen and higher myeloperoxidase activity was shown. Azithromycin 32-34 myeloperoxidase Homo sapiens 237-252 12712826-8 2003 Taking into account the duration of hospitalization, it was shown that the mean total costs of treatment of COPD exacerbation with azithromycin was significantly lower than that of treatment with cefoperazone (2375.9 PLN and 1663.7 PLN, respectively) (p < 0.05). Azithromycin 131-143 phospholamban Homo sapiens 232-235 12384353-3 2002 Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. Azithromycin 0-12 tumor necrosis factor Homo sapiens 27-54 12384353-3 2002 Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. Azithromycin 0-12 tumor necrosis factor Homo sapiens 56-65 12384353-3 2002 Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. Azithromycin 0-12 interleukin 1 beta Homo sapiens 68-85 12384353-3 2002 Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. Azithromycin 0-12 interleukin 1 beta Homo sapiens 87-95 12384353-3 2002 Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. Azithromycin 0-12 interleukin 6 Homo sapiens 102-106 12384353-4 2002 In Stx-injected mice, azithromycin significantly suppressed Stx-induced TNF-alpha, IL-1beta, and IL-6 levels in serum and improved the outcome as assessed by survival rate. Azithromycin 22-34 tumor necrosis factor Mus musculus 72-81 12384353-4 2002 In Stx-injected mice, azithromycin significantly suppressed Stx-induced TNF-alpha, IL-1beta, and IL-6 levels in serum and improved the outcome as assessed by survival rate. Azithromycin 22-34 interleukin 1 beta Mus musculus 83-91 12384353-4 2002 In Stx-injected mice, azithromycin significantly suppressed Stx-induced TNF-alpha, IL-1beta, and IL-6 levels in serum and improved the outcome as assessed by survival rate. Azithromycin 22-34 interleukin 6 Mus musculus 97-101 12431870-0 2002 Disposition and intracellular activity of azithromycin in human THP-1 acute monocytes. Azithromycin 42-54 GLI family zinc finger 2 Homo sapiens 64-69 12431870-5 2002 Azithromycin uptake into human THP-1 monocytes was initially linear achieving approximately 2% of the extracellular concentration. Azithromycin 0-12 GLI family zinc finger 2 Homo sapiens 31-36 12208321-7 2002 A continuous fall in chemokine and interleukin-6 serum concentrations, within the non-pathological range, accompanied a delayed down-regulation of the oxidative burst and an increase in apoptosis of neutrophils up to 28 days after the last azithromycin dose. Azithromycin 240-252 interleukin 6 Homo sapiens 35-48 12433117-2 2002 AZT is separated from its synthesis intermediates and a degradation product as well as from six unknown impurities on an XTerra RP18 column at 70 degrees C using a mobile phase consisting of acetonitrile-pH 6.5 0.2M K2HPO4-water (35:10:55, v/v/v) at 1.0 mL/min. Azithromycin 0-3 pre-mRNA processing factor 3 Homo sapiens 128-132 12435295-6 2002 (2) The oral administration of AZI inhibited the expression of IL-10 and IFN-gamma mRNA; reversed the Th2-like response in the BLM group to the Th1-like response on day 7; and decreased the exudation of inflammatory cells as well as the degree of fibrosis. Azithromycin 31-34 interleukin 10 Rattus norvegicus 63-68 12200967-8 2002 The effect of the antibiotics on the mRNA expression of alkaline phosphatase (ALP) and type I procollagen (COL) was examined in Pel cells exposed for 48 h to RXM, CAM, AZM, and EM, which exhibited strong, moderate, and weak cytocidal activity. Azithromycin 168-171 alkaline phosphatase, placental Homo sapiens 56-76 12200967-9 2002 The constitutive levels of both ALP and COL mRNA were retained in cells exposed to RXM at < or = 3 microM, CAM at < or = 10 microM, and AZM or EM at < or = 3 microM. Azithromycin 142-145 alkaline phosphatase, placental Homo sapiens 32-35 12435295-6 2002 (2) The oral administration of AZI inhibited the expression of IL-10 and IFN-gamma mRNA; reversed the Th2-like response in the BLM group to the Th1-like response on day 7; and decreased the exudation of inflammatory cells as well as the degree of fibrosis. Azithromycin 31-34 interferon gamma Rattus norvegicus 73-82 12435295-8 2002 (2) Azithromycin can inhibit the expression of IL-10 and IFN-gamma, and reverse the Th2-like response in the BLM group to a Th1-like response, and as a result, decrease the inflammatory injury as well as the degree of BLM-induced lung injury in rats. Azithromycin 4-16 interleukin 10 Rattus norvegicus 47-52 12435295-8 2002 (2) Azithromycin can inhibit the expression of IL-10 and IFN-gamma, and reverse the Th2-like response in the BLM group to a Th1-like response, and as a result, decrease the inflammatory injury as well as the degree of BLM-induced lung injury in rats. Azithromycin 4-16 interferon gamma Rattus norvegicus 57-66 11867823-11 2002 Median C reactive protein (CRP) levels declined in the AZM group from 10 to 5.4 mg/ml but remained constant in the placebo group (p<0.001). Azithromycin 55-58 C-reactive protein Homo sapiens 7-25 11901039-8 2002 Azithromycin therapy also resulted in a significant decrease of E-selectin and von Willebrand factor levels. Azithromycin 0-12 selectin E Homo sapiens 64-74 11867823-11 2002 Median C reactive protein (CRP) levels declined in the AZM group from 10 to 5.4 mg/ml but remained constant in the placebo group (p<0.001). Azithromycin 55-58 C-reactive protein Homo sapiens 27-30 11867823-13 2002 CONCLUSION: AZM in adults with CF significantly improved QOL, reduced CRP levels and the number of respiratory exacerbations, and reduced the rate of decline in lung function. Azithromycin 12-15 C-reactive protein Homo sapiens 70-73 11073759-5 2000 The likelihood of relapse was 39% versus 27% (P=.21) on azithromycin compared with clarithromycin, respectively. Azithromycin 56-68 H3 histone pseudogene 16 Homo sapiens 46-51 11389120-1 2001 We investigated the effects of azithromycin and clarithromycin, two antibiotics that possess a broad spectrum of antimicrobial activity (including antimycobacterial activity), on interleukin-8 (IL-8) release from human whole blood leucocytes and lung macrophages. Azithromycin 31-43 C-X-C motif chemokine ligand 8 Homo sapiens 179-192 11389120-1 2001 We investigated the effects of azithromycin and clarithromycin, two antibiotics that possess a broad spectrum of antimicrobial activity (including antimycobacterial activity), on interleukin-8 (IL-8) release from human whole blood leucocytes and lung macrophages. Azithromycin 31-43 C-X-C motif chemokine ligand 8 Homo sapiens 194-198 11389120-3 2001 Incubation of alveolar macrophages with different concentrations of azithromycin or clarithromycin modified IL-8 production: it increased at a drug concentration of 4 mg/L and decreased at concentration of 400 mg/L. Azithromycin 68-80 C-X-C motif chemokine ligand 8 Homo sapiens 108-112 11389120-4 2001 Our findings suggest that azithromycin and clarithromycin may alter IL-8 production, thus enhancing the clinical effectiveness of these antibiotics. Azithromycin 26-38 C-X-C motif chemokine ligand 8 Homo sapiens 68-72 11714218-9 2001 Administration of azithromycin may have caused the increased cyclosporine concentrations in this patient through p-glycoprotein inhibition and/or competition for biliary excretion. Azithromycin 18-30 ATP binding cassette subfamily B member 1 Homo sapiens 113-127 11015162-5 2000 OBJECTIVE: To compare the rate of M. avium complex infection in patients with increased CD4(+) cell counts who receive azithromycin and those receiving placebo. Azithromycin 119-131 CD4 molecule Homo sapiens 88-91 10853849-6 2000 There were significant (p<0.05) pre- to post-exposure increases in total cells, neutrophils, IL-6 and IL-8 in both the azithromycin and placebo arms. Azithromycin 122-134 interleukin 6 Homo sapiens 96-100 10847234-5 2000 RESULTS: The mean transplacental transfers (TPT(SS)) for erythromycin, roxithromycin and azithromycin were 3.0%, 4.3% and 2.6%, respectively, calculated as the ratio between the steady state concentrations in fetal venous and maternal arterial sides. Azithromycin 89-101 limb development membrane protein 1 Homo sapiens 44-47 10839761-4 2000 Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Azithromycin 0-12 C-reactive protein Homo sapiens 72-90 10839761-4 2000 Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Azithromycin 0-12 C-reactive protein Homo sapiens 92-95 10839761-4 2000 Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Azithromycin 0-12 interleukin 6 Homo sapiens 118-122 10839761-4 2000 Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Azithromycin 0-12 tumor necrosis factor Homo sapiens 124-151 10853849-6 2000 There were significant (p<0.05) pre- to post-exposure increases in total cells, neutrophils, IL-6 and IL-8 in both the azithromycin and placebo arms. Azithromycin 122-134 C-X-C motif chemokine ligand 8 Homo sapiens 105-109 10390202-8 1999 However, an increase in the t1/2beta or AUC, which is also observed with other semisynthetic macrolides (e.g., azithromycin), does seem to be not clinically relevant if one takes into account both the high therapeutic indices of these antibiotics and the usually short duration of therapy. Azithromycin 111-123 interleukin 1 receptor like 1 Homo sapiens 28-36 10766581-4 2000 METHODS: We conducted a multicenter, double-blind, randomized trial of treatment with azithromycin (1200 mg weekly) as compared with placebo in HIV-infected patients whose CD4+ cell counts had increased from less than 50 to more than 100 per cubic millimeter in response to antiretroviral therapy. Azithromycin 86-98 CD4 molecule Homo sapiens 172-175 10766581-13 2000 CONCLUSIONS: Azithromycin prophylaxis can safely be withheld in HIV-infected patients whose CD4+ cell counts have increased to more than 100 cells per cubic millimeter in response to antiretroviral therapy. Azithromycin 13-25 CD4 molecule Homo sapiens 92-95 11798706-8 1999 The level of protein and mRNA of TNFalpha, TGF-beta in lung tissue and alveolar macrophage was increased in the early stage of pulmonary fibrosis and reduced after treatment with azithromycin (P < 0.05). Azithromycin 179-191 tumor necrosis factor Rattus norvegicus 33-41 11798706-8 1999 The level of protein and mRNA of TNFalpha, TGF-beta in lung tissue and alveolar macrophage was increased in the early stage of pulmonary fibrosis and reduced after treatment with azithromycin (P < 0.05). Azithromycin 179-191 transforming growth factor, beta 1 Rattus norvegicus 43-51 11798706-10 1999 Azithromycin reduced the degree of alveolitis and fibrosis through inhibition of the activity of NF-kappaB and the expression of TNFalpha, TGF-beta mRNA and lowering the level of protein in alveolar macrophage and lung tissue in the early stage of pulmonary fibrosis. Azithromycin 0-12 tumor necrosis factor Rattus norvegicus 129-137 11798706-10 1999 Azithromycin reduced the degree of alveolitis and fibrosis through inhibition of the activity of NF-kappaB and the expression of TNFalpha, TGF-beta mRNA and lowering the level of protein in alveolar macrophage and lung tissue in the early stage of pulmonary fibrosis. Azithromycin 0-12 transforming growth factor, beta 1 Rattus norvegicus 139-147 10874380-5 1999 If azithromycin prophylaxis for M. avium complex is begun after the CD4 declines to 50/mm3, costs and quality-adjusted survival increase to approximately $44,040 and 42.78 months, respectively, for an incremental cost-effectiveness ratio of $25,000/QALY compared with no M. avium complex prophylaxis. Azithromycin 3-15 CD4 molecule Homo sapiens 68-71 10874380-8 1999 CONCLUSIONS: Azithromycin prophylaxis, begun after the CD4 count has declined to 50/mm3, is the most cost-effective M. avium complex prophylaxis strategy. Azithromycin 13-25 CD4 molecule Homo sapiens 55-58 10221415-7 1999 For azithromycin, the most interesting results were for IL-1alpha (decrease in 100% of individuals) and for TNF-alpha (decrease in 100% of individuals). Azithromycin 4-16 interleukin 1 alpha Homo sapiens 56-65 10223943-9 1999 We conclude that (i) the control exerted by gamma interferon on intracellular multiplication of Listeria in THP-1 macrophages is dependent on the production of nitric oxide and hydrogen peroxide; (ii) intracellular Listeria may become insensitive to ampicillin in macrophages exposed to gamma interferon because the increase in reactive oxygen and nitrogen intermediates already controls bacterial growth; and (iii) azithromycin and still more sparfloxacin cooperate efficiently with gamma interferon, one of the main cellular host defenses in Listeria infection. Azithromycin 416-428 GLI family zinc finger 2 Homo sapiens 108-113 10348770-2 1999 Here it is shown that the Escherichia coli msbB mutant, which elaborates defective, penta-acylated lipid A, is practically as resistant to a representative set of hydrophobic solutes (rifampin, fusidic acid, erythromycin, clindamycin, and azithromycin) as the parent-type control strain. Azithromycin 239-251 lipid A biosynthesis (KDO)2-(lauroyl)-lipid IVA acyltransferase Escherichia coli 43-47 10221415-7 1999 For azithromycin, the most interesting results were for IL-1alpha (decrease in 100% of individuals) and for TNF-alpha (decrease in 100% of individuals). Azithromycin 4-16 tumor necrosis factor Homo sapiens 108-117 9145822-0 1997 Effect of combination therapy of rifampicin and azithromycin on TNF levels during a rat model of chronic osteomyelitis. Azithromycin 48-60 tumor necrosis factor Rattus norvegicus 64-67 10052900-4 1998 Assay of total cell phospholipids and cholesterol showed significant increases in cells exposed to > or = 1 to 5 mg/L of azithromycin in association with hyperactivity of the lysosomal enzyme cathepsin B. Azithromycin 124-136 cathepsin B Rattus norvegicus 195-206 9727572-12 1998 When not contraindicated, starting azithromycin or rifabutin when the patient"s CD4 count is between 50 and 75 x 10(6) cells/l is the most cost-effective strategy. Azithromycin 35-47 CD4 molecule Homo sapiens 80-83 9292586-7 1997 RESULTS: For patients with AIDS and those having CD4 counts <75 cells/mm3, azithromycin, clarithromycin, and rifabutin prophylaxis increased lifetime per person MAC-related costs by $994, $2,117, and $2,185 U.S., respectively. Azithromycin 78-90 CD4 molecule Homo sapiens 49-52 9292586-13 1997 In the context of Centers for Disease Control and Prevention (CDC) recommendations to use prophylaxis in patients with CD4 counts <75 cells/mm3, azithromycin represents the best value and is most cost-effective when used in patients with CD4 counts <25 cells/mm3. Azithromycin 148-160 CD4 molecule Homo sapiens 119-122 9292586-13 1997 In the context of Centers for Disease Control and Prevention (CDC) recommendations to use prophylaxis in patients with CD4 counts <75 cells/mm3, azithromycin represents the best value and is most cost-effective when used in patients with CD4 counts <25 cells/mm3. Azithromycin 148-160 CD4 molecule Homo sapiens 241-244 8547740-17 1995 Azithromycin, a member of the new azalide class, has to date produced fewer clinically significant interactions than other azalides with any agent that is cleared through the CYP3A system. Azithromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-180 8830663-0 1996 Hyperactivity of cathepsin B and other lysosomal enzymes in fibroblasts exposed to azithromycin, a dicationic macrolide antibiotic with exceptional tissue accumulation. Azithromycin 83-95 cathepsin B Homo sapiens 17-28 8539079-4 1995 The azithromycin in vitro activity on Chl. Azithromycin 4-16 chordin like 1 Homo sapiens 38-41 7952797-8 1994 At subinhibitory extracellular concentrations of azithromycin as low as 0.03 mg/l (MIC = 1 mg/l), a significant reduction in bacterial viability was observed, thus demonstrating antibacterial activity of the intracellularly enriched antibiotic. Azithromycin 49-61 growth differentiation factor 15 Homo sapiens 83-90 8158029-5 1994 Therefore, a significant reduction in the number of viable bacteria was observed in blood, liver, and spleen of mice treated with a combination of GM-CSF and azithromycin or amikacin compared with control mice and those treated with GM-CSF or antimicrobials alone. Azithromycin 158-170 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 233-239 1667256-3 1991 We now report that stimulation of macrophages either with recombinant human gamma interferon (IFN-gamma, 10(2) U/ml) or with recombinant human TNF-alpha (10(2) U/ml) resulted in an increase in the intracellular concentration of azithromycin by approximately 200% within 3 h, compared with the concentration in unstimulated macrophages. Azithromycin 228-240 interferon gamma Homo sapiens 76-103 8280403-8 1993 Gastrointestinal reactions represent the most frequent disturbance, occurring in 15 to 20% of patients on erythromycins and in 5% or fewer patients treated with some recently developed macrolide derivatives that seldom or never induce endogenous release of motilin, such as roxithromycin, clarithromycin, dirithromycin, azithromycin and rikamycin (rokitamycin). Azithromycin 320-332 motilin Homo sapiens 257-264 1667256-3 1991 We now report that stimulation of macrophages either with recombinant human gamma interferon (IFN-gamma, 10(2) U/ml) or with recombinant human TNF-alpha (10(2) U/ml) resulted in an increase in the intracellular concentration of azithromycin by approximately 200% within 3 h, compared with the concentration in unstimulated macrophages. Azithromycin 228-240 tumor necrosis factor Homo sapiens 143-152 34478690-0 2022 Effects of intranasal azithromycin on features of cigarette smoke-induced lung inflammation. Azithromycin 22-34 citrate synthase Homo sapiens 50-65 33806962-7 2021 After screening for antimicrobial resistance (AMR) genes, we found a ribosomal protection protein, Msr(D), in these highly azithromycin resistant nonpathogenic strains. Azithromycin 123-135 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 99-102 34694885-5 2022 Introducing the ramAp and the truncated ISEcp1 into E. coli have resulted in elevated expression of efflux pump genes and elevated MICs to chloramphenicol, azithromycin, nalidixic acid, ciprofloxacin, sulfamethoxazole, trimethoprim, tetracycline, and tigecycline. Azithromycin 156-168 ISEcp1 Escherichia coli 40-46 2154437-4 1990 Rate constants and the time for 10% decay (T1/10) were determined for both azithromycin and erythromycin A at pH2 using various levels of acetonitrile cosolvent and constant ionic strength. Azithromycin 75-87 CD5 molecule Homo sapiens 43-48 2154437-6 1990 In solution at 37 degrees C and pH2 with ionic strength mu = 0.02, azithromycin was degraded with a T1/10 of 20.1 min while erythromycin underwent 10% decay in only 3.7 sec. Azithromycin 67-79 CD5 molecule Homo sapiens 100-105 33822092-0 2021 Dual azithromycin/ceftriaxone therapy for gonorrhoea in PrEP cohorts results in levels of macrolide consumption that exceed resistance thresholds by up to 7-fold. Azithromycin 5-17 prolyl endopeptidase Homo sapiens 56-60 33806340-5 2021 A significant association (p value < 0.05) was observed between the multidrug efflux pump (AcrA) and resistance to beta-lactams and the aminoglycoside acetyl transferase gene (aac-6"-Ib) gene and resistance to ciprofloxacin, azithromycin and beta-lactams (except for aztreonam). Azithromycin 225-237 aminoglycoside N(6')-acetyltransferase Klebsiella pneumoniae 176-185 12907132-4 2003 The LPS-enhanced PGE2 synthesis and the expression of cPLA2 and COX-2 mRNAs were inhibited by clarithromycin, azithromycin and dexamethasone in PMNLs and MNLs. Azithromycin 110-122 phospholipase A2 group IVA Homo sapiens 54-59 12907132-4 2003 The LPS-enhanced PGE2 synthesis and the expression of cPLA2 and COX-2 mRNAs were inhibited by clarithromycin, azithromycin and dexamethasone in PMNLs and MNLs. Azithromycin 110-122 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 12907132-5 2003 The mRNA expression of COX-1 in PMNLs was decreased by clarithromycin and azithromycin. Azithromycin 74-86 mitochondrially encoded cytochrome c oxidase I Homo sapiens 23-28 34478690-6 2022 AZT alone and in combination with DEX significantly inhibited the CS (E)-induced expression of mesenchymal protein markers and the regulatory protein beta-catenin. Azithromycin 0-3 catenin beta 1 Homo sapiens 150-162 34478690-7 2022 Furthermore, AZT by itself or in combination with DEX significantly suppressed CS-induced expression of the proinflammatory cytokine TNFalpha and prevented p-NFkB. Azithromycin 13-16 tumor necrosis factor Homo sapiens 133-141 34478690-8 2022 Mechanistically, AZT restored the CS-induced reduction in anti-oxidant transcription factor NRF2 and upregulated HDAC2 levels, thereby repressing inflammatory gene expression. Azithromycin 17-20 NFE2 like bZIP transcription factor 2 Homo sapiens 92-96 34478690-8 2022 Mechanistically, AZT restored the CS-induced reduction in anti-oxidant transcription factor NRF2 and upregulated HDAC2 levels, thereby repressing inflammatory gene expression. Azithromycin 17-20 histone deacetylase 2 Homo sapiens 113-118 34088250-0 2022 NSAIDs/Nitazoxanide/Azithromycin Repurposed for COVID-19: Potential Mitigation of the Cytokine Storm Interleukin-6 Amplifier via Immunomodulatory Effects. Azithromycin 20-32 interleukin 6 Homo sapiens 101-114 34943763-0 2021 In Vitro Synergism of Azithromycin Combination with Antibiotics against OXA-48-Producing Klebsiella pneumoniae Clinical Isolates. Azithromycin 22-34 OXA-48 Klebsiella pneumoniae 72-78 34819259-7 2022 AZI pretreatment elevated the levels of IL-4, IL-6, and IL-17A in the ear skin of AD model mice, but it increased serum TNF-alpha and IL-6. Azithromycin 0-3 interleukin 17A Mus musculus 56-62 34819259-7 2022 AZI pretreatment elevated the levels of IL-4, IL-6, and IL-17A in the ear skin of AD model mice, but it increased serum TNF-alpha and IL-6. Azithromycin 0-3 tumor necrosis factor Mus musculus 120-129 34819259-7 2022 AZI pretreatment elevated the levels of IL-4, IL-6, and IL-17A in the ear skin of AD model mice, but it increased serum TNF-alpha and IL-6. Azithromycin 0-3 interleukin 6 Mus musculus 134-138 34843998-6 2022 iHMGEC cultured in serum-containing medium under hypoxia or with azithromycin increases DNAse 2 activity, a biomarker of terminal differentiation in sebocytes. Azithromycin 65-77 deoxyribonuclease 2, lysosomal Homo sapiens 88-95 34819259-7 2022 AZI pretreatment elevated the levels of IL-4, IL-6, and IL-17A in the ear skin of AD model mice, but it increased serum TNF-alpha and IL-6. Azithromycin 0-3 interleukin 4 Mus musculus 40-44 34819259-7 2022 AZI pretreatment elevated the levels of IL-4, IL-6, and IL-17A in the ear skin of AD model mice, but it increased serum TNF-alpha and IL-6. Azithromycin 0-3 interleukin 6 Mus musculus 46-50 34943763-13 2021 In conclusion, the combination of azithromycin and colistin may be an alternative strategy in dealing with blaOXA-48-carrying K. pneumoniae infection during a recent shortage of newly effective antibiotic development. Azithromycin 34-46 OXA-48 Klebsiella pneumoniae 107-116 34803671-0 2021 Azithromycin Attenuates Bleomycin-Induced Pulmonary Fibrosis Partly by Inhibiting the Expression of LOX and LOXL-2. Azithromycin 0-12 lysyl oxidase Mus musculus 100-103 34957746-5 2021 In the GINA report, azithromycin can be recommended as an add-on therapy in patients with uncontrolled non-T2 severe asthma despite high-dose inhaled corticosteroid/ long-acting beta2-agonist/long-acting antimuscariniric treatments, or in T2 severe asthma patients whose asthma is not under control despite biologic therapy. Azithromycin 20-32 ATPase H+ transporting V0 subunit a2 Homo sapiens 178-183 34802170-10 2022 The combination therapy with azithromycin was another independent predictor of a serious ADR. Azithromycin 29-41 aldo-keto reductase family 1 member B Homo sapiens 89-92 34781403-10 2021 Moreover, there was a significant tumor necrosis factor-alpha (TNF-alpha) decline (p < 0.01) and interleukin-10 (IL-10) elevation (p < 0.01) in the spinal cord tissue of the AZM-treated group compared with the control groups 28 days post-SCI. Azithromycin 174-177 tumor necrosis factor Rattus norvegicus 34-61 34781403-10 2021 Moreover, there was a significant tumor necrosis factor-alpha (TNF-alpha) decline (p < 0.01) and interleukin-10 (IL-10) elevation (p < 0.01) in the spinal cord tissue of the AZM-treated group compared with the control groups 28 days post-SCI. Azithromycin 174-177 tumor necrosis factor Rattus norvegicus 63-72 34781403-10 2021 Moreover, there was a significant tumor necrosis factor-alpha (TNF-alpha) decline (p < 0.01) and interleukin-10 (IL-10) elevation (p < 0.01) in the spinal cord tissue of the AZM-treated group compared with the control groups 28 days post-SCI. Azithromycin 174-177 interleukin 10 Rattus norvegicus 97-111 34781403-10 2021 Moreover, there was a significant tumor necrosis factor-alpha (TNF-alpha) decline (p < 0.01) and interleukin-10 (IL-10) elevation (p < 0.01) in the spinal cord tissue of the AZM-treated group compared with the control groups 28 days post-SCI. Azithromycin 174-177 interleukin 10 Rattus norvegicus 113-118 34803671-6 2021 Meanwhile, expression of lysyl oxidase (LOX) and lysyl oxidase-like protein (LOXL)-2 in the lung tissue of mice after AZM treatment was significantly lower than in the BLM group. Azithromycin 118-121 lysyl oxidase Mus musculus 25-38 34803671-6 2021 Meanwhile, expression of lysyl oxidase (LOX) and lysyl oxidase-like protein (LOXL)-2 in the lung tissue of mice after AZM treatment was significantly lower than in the BLM group. Azithromycin 118-121 lysyl oxidase Mus musculus 40-43 34803671-0 2021 Azithromycin Attenuates Bleomycin-Induced Pulmonary Fibrosis Partly by Inhibiting the Expression of LOX and LOXL-2. Azithromycin 0-12 lysyl oxidase-like 2 Mus musculus 108-114 34803671-6 2021 Meanwhile, expression of lysyl oxidase (LOX) and lysyl oxidase-like protein (LOXL)-2 in the lung tissue of mice after AZM treatment was significantly lower than in the BLM group. Azithromycin 118-121 lysyl oxidase-like 2 Mus musculus 49-84 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 transforming growth factor, beta 1 Mus musculus 66-75 34803671-5 2021 AZM effectively reduced the expression of alpha-smooth muscle actin (SMA) and type I collagen. Azithromycin 0-3 immunoglobulin mu binding protein 2 Mus musculus 69-72 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 mitogen-activated protein kinase 8 Mus musculus 85-88 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 jun proto-oncogene Mus musculus 89-94 34245078-8 2021 Utilization of azithromycin and all systemic antibiotics decreased continuously from March 2-8 until June to levels considerably lower compared to 2019 (June 22-28: azithromycin: -55%, all systemic antibiotics: -27%). Azithromycin 15-27 membrane associated ring-CH-type finger 2 Homo sapiens 85-94 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 actin alpha 2, smooth muscle, aorta Mus musculus 141-146 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 lysyl oxidase Mus musculus 165-168 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 35-38 lysyl oxidase-like 2 Mus musculus 173-179 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 transforming growth factor, beta 1 Mus musculus 66-75 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 mitogen-activated protein kinase 8 Mus musculus 85-88 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 jun proto-oncogene Mus musculus 89-94 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 actin alpha 2, smooth muscle, aorta Mus musculus 141-146 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 lysyl oxidase Mus musculus 165-168 34803671-7 2021 In addition, this study found that AZM significantly inhibits the TGF-beta1/Smad and JNK/c-Jun signaling pathways in vivo, and expression of a-SMA, type I collagen, LOX and LOXL-2 in the lung tissue of mice treated with AZM was significantly lower than that in the BLM group. Azithromycin 220-223 lysyl oxidase-like 2 Mus musculus 173-179 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 lysyl oxidase Mus musculus 58-61 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 lysyl oxidase-like 2 Mus musculus 63-69 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 mitogen-activated protein kinase 8 Mus musculus 74-77 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 jun proto-oncogene Mus musculus 78-83 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 transforming growth factor, beta 1 Mus musculus 106-115 34803671-8 2021 In vitro, AZM also effectively inhibited type I collagen, LOX, LOXL-2 and JNK-c-Jun signaling pathways in TGF-beta1-stimulated primary mouse fibroblasts, and this effect was similar to that of a JNK-specific inhibitor (SP600125). Azithromycin 10-13 mitogen-activated protein kinase 8 Mus musculus 195-198 34803671-9 2021 In conclusion, AZM effectively attenuated BLM-induced PF in mice, which may play a role by partially inhibiting the JNK/c-Jun and TGF-beta1/Smad signaling pathways and reducing production of LOX and LOXL2. Azithromycin 15-18 mitogen-activated protein kinase 8 Mus musculus 116-119 34803671-9 2021 In conclusion, AZM effectively attenuated BLM-induced PF in mice, which may play a role by partially inhibiting the JNK/c-Jun and TGF-beta1/Smad signaling pathways and reducing production of LOX and LOXL2. Azithromycin 15-18 jun proto-oncogene Mus musculus 120-125 34803671-9 2021 In conclusion, AZM effectively attenuated BLM-induced PF in mice, which may play a role by partially inhibiting the JNK/c-Jun and TGF-beta1/Smad signaling pathways and reducing production of LOX and LOXL2. Azithromycin 15-18 transforming growth factor, beta 1 Mus musculus 130-139 34803671-9 2021 In conclusion, AZM effectively attenuated BLM-induced PF in mice, which may play a role by partially inhibiting the JNK/c-Jun and TGF-beta1/Smad signaling pathways and reducing production of LOX and LOXL2. Azithromycin 15-18 lysyl oxidase Mus musculus 191-194 34803671-9 2021 In conclusion, AZM effectively attenuated BLM-induced PF in mice, which may play a role by partially inhibiting the JNK/c-Jun and TGF-beta1/Smad signaling pathways and reducing production of LOX and LOXL2. Azithromycin 15-18 lysyl oxidase-like 2 Mus musculus 199-204 34310083-11 2021 Azithromycin concentration was positively correlated with IL-8 (r = 0.38, p = 0.03), IL1a (r = 0.39, p = 0.03), and IL-1b (r = 0.36, p = 0.04) in amniotic fluid. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 58-62 34310083-11 2021 Azithromycin concentration was positively correlated with IL-8 (r = 0.38, p = 0.03), IL1a (r = 0.39, p = 0.03), and IL-1b (r = 0.36, p = 0.04) in amniotic fluid. Azithromycin 0-12 interleukin 1 alpha Homo sapiens 85-89 34310083-11 2021 Azithromycin concentration was positively correlated with IL-8 (r = 0.38, p = 0.03), IL1a (r = 0.39, p = 0.03), and IL-1b (r = 0.36, p = 0.04) in amniotic fluid. Azithromycin 0-12 interleukin 1 beta Homo sapiens 116-121 34600916-0 2021 Azithromycin modulates Teff/Treg balance in retinal inflammation via the mTOR signaling pathway. Azithromycin 0-12 mechanistic target of rapamycin kinase Homo sapiens 73-77 34600916-8 2021 Additionally, Azithromycin suppressed the proliferation and activation of CD4+T cells, and induced the apoptosis of CD4+CD44+ memory T and CD4+CXCR3+ Th1 cells. Azithromycin 14-26 CD4 molecule Homo sapiens 74-77 34600916-8 2021 Additionally, Azithromycin suppressed the proliferation and activation of CD4+T cells, and induced the apoptosis of CD4+CD44+ memory T and CD4+CXCR3+ Th1 cells. Azithromycin 14-26 CD4 molecule Homo sapiens 116-119 34600916-8 2021 Additionally, Azithromycin suppressed the proliferation and activation of CD4+T cells, and induced the apoptosis of CD4+CD44+ memory T and CD4+CXCR3+ Th1 cells. Azithromycin 14-26 CD44 molecule (Indian blood group) Homo sapiens 120-124 34600916-8 2021 Additionally, Azithromycin suppressed the proliferation and activation of CD4+T cells, and induced the apoptosis of CD4+CD44+ memory T and CD4+CXCR3+ Th1 cells. Azithromycin 14-26 CD4 molecule Homo sapiens 139-142 34600916-8 2021 Additionally, Azithromycin suppressed the proliferation and activation of CD4+T cells, and induced the apoptosis of CD4+CD44+ memory T and CD4+CXCR3+ Th1 cells. Azithromycin 14-26 C-X-C motif chemokine receptor 3 Homo sapiens 143-148 34600916-9 2021 Mechanistically, we proved that Azithromycin could regulate Teff/Treg balance by inhibiting the phosphorylation of S6 ribosomal protein, a downstream target of mammalian target of rapamycin (mTOR). Azithromycin 32-44 mechanistic target of rapamycin kinase Homo sapiens 160-189 34600916-9 2021 Mechanistically, we proved that Azithromycin could regulate Teff/Treg balance by inhibiting the phosphorylation of S6 ribosomal protein, a downstream target of mammalian target of rapamycin (mTOR). Azithromycin 32-44 mechanistic target of rapamycin kinase Homo sapiens 191-195 34600916-10 2021 Together, our findings revealed that Azithromycin alleviated EAU by regulating the Teff/Treg balance through the mTOR signalling pathway, suggesting that Azithromycin could be a promising therapeutic candidate for AU. Azithromycin 37-49 mechanistic target of rapamycin kinase Homo sapiens 113-117 34600916-10 2021 Together, our findings revealed that Azithromycin alleviated EAU by regulating the Teff/Treg balance through the mTOR signalling pathway, suggesting that Azithromycin could be a promising therapeutic candidate for AU. Azithromycin 154-166 mechanistic target of rapamycin kinase Homo sapiens 113-117 34610107-0 2021 Combination of Kaempferol and Azithromycin attenuates Staphylococcus aureus induced osteomyelitis via anti-biofilm effect and inhibiting phosphorylation of ERK1/2 and SAPK. Azithromycin 30-42 mitogen activated protein kinase 3 Rattus norvegicus 156-162 34664264-0 2022 Azithromycin alleviates the severity of rheumatoid arthritis by targeting the UPR component GRP78. Azithromycin 0-12 heat shock protein family A (Hsp70) member 5 Homo sapiens 92-97 34664264-4 2022 In vitro and in vivo assays were performed to examine the effects of AZM-mediated blockade of glucose-regulated protein 78 (GRP78). Azithromycin 69-72 heat shock protein family A (Hsp70) member 5 Homo sapiens 94-122 34664264-4 2022 In vitro and in vivo assays were performed to examine the effects of AZM-mediated blockade of glucose-regulated protein 78 (GRP78). Azithromycin 69-72 heat shock protein family A (Hsp70) member 5 Homo sapiens 124-129 34664264-6 2022 Identification and characterization of the binding of AZM to GRP78 was performed using drug affinity responsive target stability assays, proteomics and cellular thermal shift assays. Azithromycin 54-57 heat shock protein family A (Hsp70) member 5 Homo sapiens 61-66 34664264-7 2022 AZM-mediated inhibition of GRP78 and the dependence of the antiarthritic activity of AZM on GRP78 were assessed. Azithromycin 0-3 heat shock protein family A (Hsp70) member 5 Homo sapiens 27-32 34664264-7 2022 AZM-mediated inhibition of GRP78 and the dependence of the antiarthritic activity of AZM on GRP78 were assessed. Azithromycin 85-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 92-97 34664264-11 2022 GRP78 was identified as a novel target of AZM. Azithromycin 42-45 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 34664264-12 2022 AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes. Azithromycin 0-3 heat shock protein family A (Hsp70) member 5 Homo sapiens 85-90 34664264-12 2022 AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes. Azithromycin 0-3 DNA damage inducible transcript 3 Homo sapiens 152-176 34664264-12 2022 AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes. Azithromycin 0-3 DNA damage inducible transcript 3 Homo sapiens 178-182 34664264-12 2022 AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes. Azithromycin 0-3 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 212-253 34664264-12 2022 AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes. Azithromycin 0-3 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 255-260 34664264-13 2022 Furthermore, deletion of GRP78 abolished the antiarthritic activity of AZM. Azithromycin 71-74 heat shock protein family A (Hsp70) member 5 Homo sapiens 25-30 34610107-0 2021 Combination of Kaempferol and Azithromycin attenuates Staphylococcus aureus induced osteomyelitis via anti-biofilm effect and inhibiting phosphorylation of ERK1/2 and SAPK. Azithromycin 30-42 mitogen-activated protein kinase 9 Rattus norvegicus 167-171 34380260-8 2021 Moreover, we also demonstrated an increase in the AChE activity followed by a reduction in the neuromasts of the head when zebrafish were exposed to the mixture AZT + HCQ. Azithromycin 161-164 acetylcholinesterase Danio rerio 50-54 34698079-7 2021 In cells cultured with 10 microg/mL azithromycin, the ALPase activity and mineralized nodule formation decreased, while the type I collagen, bone sialoprotein, osteocalcin, and osteopontin mRNA expression as well as osteopontin and phosphorylated osteopontin levels increased. Azithromycin 36-48 bone gamma-carboxyglutamate protein 2 Mus musculus 160-171 34698079-7 2021 In cells cultured with 10 microg/mL azithromycin, the ALPase activity and mineralized nodule formation decreased, while the type I collagen, bone sialoprotein, osteocalcin, and osteopontin mRNA expression as well as osteopontin and phosphorylated osteopontin levels increased. Azithromycin 36-48 secreted phosphoprotein 1 Mus musculus 177-188 34698079-7 2021 In cells cultured with 10 microg/mL azithromycin, the ALPase activity and mineralized nodule formation decreased, while the type I collagen, bone sialoprotein, osteocalcin, and osteopontin mRNA expression as well as osteopontin and phosphorylated osteopontin levels increased. Azithromycin 36-48 secreted phosphoprotein 1 Mus musculus 216-227 34698079-7 2021 In cells cultured with 10 microg/mL azithromycin, the ALPase activity and mineralized nodule formation decreased, while the type I collagen, bone sialoprotein, osteocalcin, and osteopontin mRNA expression as well as osteopontin and phosphorylated osteopontin levels increased. Azithromycin 36-48 secreted phosphoprotein 1 Mus musculus 247-258 34698079-8 2021 These results suggest that a high azithromycin concentration (10 microg/mL) suppresses mineralized nodule formation by decreasing ALPase activity and increasing osteopontin production, whereas low concentrations (<=l.0 microg/mL) have no effect on osteogenic function in osteoblastic MC3T3-E1 cells. Azithromycin 34-46 secreted phosphoprotein 1 Mus musculus 161-172 34584985-9 2021 Azithromycin, which also belongs to the class of MAs, can be a promising therapeutic option for MPD in case of clarithromycin intolerance. Azithromycin 0-12 mevalonate diphosphate decarboxylase Homo sapiens 96-99 34719987-2 2021 METHODS: Five databases (PubMed, Google Scholar, Trip, Medline, and Clinical Key) were searched to identify randomized clinical trials with patients exposed to azithromycin or clarithromycin in combination with a beta-lactam. Azithromycin 160-172 TRAF interacting protein Homo sapiens 49-53 34533110-3 2022 PURPOSE AND METHOD: The present study was undertaken to explore the cytotoxicity and anticancer effects of DOXY and AZI on human GBM U87 cells via 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), Hoechst, Annexin V-FITC/PI, and clonogenic assays. Azithromycin 116-119 annexin A5 Homo sapiens 226-235 34541478-9 2021 Most studies investigated azithromycin as Intermittent Preventive Treatment in Pregnancy (IPTp) for malaria. Azithromycin 26-38 tRNA isopentenyltransferase 1 Homo sapiens 90-94 34539665-9 2021 Remarkably, C4BP-IgM restored susceptibility to azithromycin of two azithromycin-resistant clinical gonococcal strains because of overexpression of the MtrC-MtrD-MtrE efflux pump. Azithromycin 48-60 complement component 4 binding protein alpha Homo sapiens 12-16 34479861-1 2022 OBJECTIVE: To assess whether intermittent preventive treatment of pregnant women (IPTp) with sulfadoxine-pyrimethamine (SP) and azithromycin (AZI) in a malaria-endemic area leads to sustained gains in linear growth and development in their offspring. Azithromycin 128-140 antizyme inhibitor 1 Homo sapiens 142-145 34539665-9 2021 Remarkably, C4BP-IgM restored susceptibility to azithromycin of two azithromycin-resistant clinical gonococcal strains because of overexpression of the MtrC-MtrD-MtrE efflux pump. Azithromycin 68-80 complement component 4 binding protein alpha Homo sapiens 12-16 34367377-14 2021 Serum protein expressions of IL-17 (p = 0.0017), IL-18 (p = 0.0036), IFN-gamma (p = 0.0102), and MMP-9 (p = 0.0194) were significantly decreased in the allograft+tacrolimus+azithromycin group compared to the allograft group. Azithromycin 173-185 interleukin 17A Mus musculus 29-34 34540066-1 2021 OBJECTIVE: To analyze the expression levels of total serum interleukin (IL)-6 and tumor necrosis factor (TNF)-C in children with bronchopneumonia treated by methylprednisolone in combination with azithromycin. Azithromycin 196-208 lymphotoxin beta Homo sapiens 82-111 34148466-8 2021 In mild-to-moderate Crohn"s disease, azithromycin+metronidazole (AZ+MET) (n=35) compared to metronidazole (MET) alone (n=38) did not induce a significantly different response (PCDAI drop >=12.5 points or remission) (p=0.07). Azithromycin 37-49 SAFB like transcription modulator Homo sapiens 65-71 34229290-3 2021 METHODS: 1219 COPD patients enrolled in either the simvastatin for the prevention of exacerbations in moderate-to severe COPD Trial (STATCOPE) or azithromycin for prevention of exacerbations of COPD trial (MACRO) were analyzed. Azithromycin 146-158 COPD Homo sapiens 14-18 34540066-0 2021 Total serum IL-6 and TNF-C levels in children with bronchopneumonia following treatment with methylprednisolone in combination with azithromycin. Azithromycin 132-144 interleukin 6 Homo sapiens 12-16 34540066-0 2021 Total serum IL-6 and TNF-C levels in children with bronchopneumonia following treatment with methylprednisolone in combination with azithromycin. Azithromycin 132-144 lymphotoxin beta Homo sapiens 21-26 34540066-1 2021 OBJECTIVE: To analyze the expression levels of total serum interleukin (IL)-6 and tumor necrosis factor (TNF)-C in children with bronchopneumonia treated by methylprednisolone in combination with azithromycin. Azithromycin 196-208 interleukin 6 Homo sapiens 59-77 34367377-14 2021 Serum protein expressions of IL-17 (p = 0.0017), IL-18 (p = 0.0036), IFN-gamma (p = 0.0102), and MMP-9 (p = 0.0194) were significantly decreased in the allograft+tacrolimus+azithromycin group compared to the allograft group. Azithromycin 173-185 interleukin 18 Mus musculus 49-54 34367377-14 2021 Serum protein expressions of IL-17 (p = 0.0017), IL-18 (p = 0.0036), IFN-gamma (p = 0.0102), and MMP-9 (p = 0.0194) were significantly decreased in the allograft+tacrolimus+azithromycin group compared to the allograft group. Azithromycin 173-185 interferon gamma Mus musculus 69-78 34367377-14 2021 Serum protein expressions of IL-17 (p = 0.0017), IL-18 (p = 0.0036), IFN-gamma (p = 0.0102), and MMP-9 (p = 0.0194) were significantly decreased in the allograft+tacrolimus+azithromycin group compared to the allograft group. Azithromycin 173-185 matrix metallopeptidase 9 Mus musculus 97-102 34356479-9 2021 In conclusion, azithromycin combinations with either linezolid, or ceftriaxone showed synergism in most of the MAC-resistant MRSA clinical isolates. Azithromycin 15-27 solute carrier family 9 member A6 Homo sapiens 125-129 34356479-7 2021 Azithromycin combinations with either linezolid, ceftriaxone, gentamicin, or cefotaxime provided synergy in 42.1%, 44.7%, 31.6% and 7.9% of the 38 MAC-MRSA isolates, respectively. Azithromycin 0-12 solute carrier family 9 member A6 Homo sapiens 151-155 34414894-7 2021 Azithromycin suppressed production of IL-4 and CXCL8 by NK and NKT-like cells, and theophylline inhibited IL-4 synthesis by these lymphocytes. Azithromycin 0-12 interleukin 4 Homo sapiens 38-42 34414894-8 2021 The combination of azithromycin and budesonide had a more pronounced inhibitory effect on the production of IL-4 and CXCL8 by NK and NKT-like cells than the effect of these drugs alone. Azithromycin 19-31 C-X-C motif chemokine ligand 8 Homo sapiens 117-122 34414894-7 2021 Azithromycin suppressed production of IL-4 and CXCL8 by NK and NKT-like cells, and theophylline inhibited IL-4 synthesis by these lymphocytes. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 47-52 34414894-8 2021 The combination of azithromycin and budesonide had a more pronounced inhibitory effect on the production of IL-4 and CXCL8 by NK and NKT-like cells than the effect of these drugs alone. Azithromycin 19-31 interleukin 4 Homo sapiens 108-112 34068694-0 2021 Deglycosylated Azithromycin Attenuates Bleomycin-Induced Pulmonary Fibrosis via the TGF-beta1 Signaling Pathway. Azithromycin 15-27 transforming growth factor beta 1 Homo sapiens 84-93 34181666-5 2021 Mechanistically, HCQ and HCQ/AZ inhibited PD-L1 expression on tumor cells, while specifically targeting the anti-PD-1 induced increase in progenitor CD8+CD44+PD-1+TCF1+ tumor infiltrating T cells (TILs) and the generation of CD8+CD44+PD-1+ effectors. Azithromycin 29-31 CD274 molecule Sus scrofa 42-47 34106964-1 2021 BACKGROUND: Hydroxychloroquine combined with azithromycin (HCQ/AZI) has initially been used against coronavirus disease-2019 (COVID-19). Azithromycin 45-57 antizyme inhibitor 1 Homo sapiens 63-66 34104863-8 2021 The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient. Azithromycin 19-31 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 61-67 34104863-8 2021 The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient. Azithromycin 19-31 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 90-96 34104863-8 2021 The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient. Azithromycin 19-31 vitamin K epoxide reductase complex subunit 1 Homo sapiens 112-118 34527114-9 2020 All markers of vascular damage were reduced in AZT group at POST interval with overall significance (P = 0.026). Azithromycin 47-50 solute carrier family 35 member G1 Homo sapiens 60-64 34602387-0 2021 Azithromycin inhibits the production of MUC5AC in the airway mucosa of patients with bronchiectasis induced by Pseudomonas aeruginosa. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 40-46 34602387-1 2021 To explore the clinical benefits of azithromycin in the treatment of Pseudomonas aeruginosa induced bronchiectasis and to evaluate its effect on MUC5AC. Azithromycin 36-48 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 145-151 34602387-5 2021 The mRNA expression of TNF-alpha, IL-8 and IL-1beta in the azithromycin group was lower than that in the control group (P<0.05). Azithromycin 59-71 tumor necrosis factor Homo sapiens 23-32 34602387-5 2021 The mRNA expression of TNF-alpha, IL-8 and IL-1beta in the azithromycin group was lower than that in the control group (P<0.05). Azithromycin 59-71 C-X-C motif chemokine ligand 8 Homo sapiens 34-38 34602387-5 2021 The mRNA expression of TNF-alpha, IL-8 and IL-1beta in the azithromycin group was lower than that in the control group (P<0.05). Azithromycin 59-71 interleukin 1 alpha Homo sapiens 43-51 34602387-6 2021 After treatment, the protein expression of MUC5AC in the azithromycin group was lower than that in the control group (P<0.05). Azithromycin 57-69 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 43-49 34602387-10 2021 Azithromycin treatment has certain clinical benefits for patients with bronchiectasis induced by Pseudomonas aeruginosa and inhibits the MUC5AC expression. Azithromycin 0-12 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 137-143 34527114-11 2020 Plasma level of C-reactive protein (CRP) was significantly decreased in AZT group as well. Azithromycin 72-75 C-reactive protein Homo sapiens 16-34 34527114-11 2020 Plasma level of C-reactive protein (CRP) was significantly decreased in AZT group as well. Azithromycin 72-75 C-reactive protein Homo sapiens 36-39 35440370-8 2022 Co-incubation of azithromycin resulted in increased CD8+ (p = 0.007) and CD4+ (p = 0.011) IL-2. Azithromycin 17-29 CD8a molecule Homo sapiens 52-55 35440370-8 2022 Co-incubation of azithromycin resulted in increased CD8+ (p = 0.007) and CD4+ (p = 0.011) IL-2. Azithromycin 17-29 CD4 molecule Homo sapiens 73-76 35440370-8 2022 Co-incubation of azithromycin resulted in increased CD8+ (p = 0.007) and CD4+ (p = 0.011) IL-2. Azithromycin 17-29 interleukin 2 Homo sapiens 90-94 35348023-8 2022 In additional ex vivo studies, ATP-induced secretion of Muc5ac from HDM-exposed tracheal segments was inhibited by in vitro exposure to azithromycin. Azithromycin 136-148 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 56-62 35348023-9 2022 In vitro azithromycin also inhibited ATP-induced secretion of Muc5ac and Muc5b in tracheal segments from IL-13-exposed mice. Azithromycin 9-21 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 62-68 35348023-9 2022 In vitro azithromycin also inhibited ATP-induced secretion of Muc5ac and Muc5b in tracheal segments from IL-13-exposed mice. Azithromycin 9-21 mucin 5, subtype B, tracheobronchial Mus musculus 73-78 35348023-9 2022 In vitro azithromycin also inhibited ATP-induced secretion of Muc5ac and Muc5b in tracheal segments from IL-13-exposed mice. Azithromycin 9-21 interleukin 13 Mus musculus 105-110 35444552-8 2022 We performed the prediction interval to virtual screening of azithromycin impurities with high hepatotoxicity and then experimentally confirmed by liver toxicity in zebrafish and c-fos gene expression. Azithromycin 61-73 v-fos FBJ murine osteosarcoma viral oncogene homolog Ab Danio rerio 179-184 35490266-8 2022 Treatment with azithromycin significantly decreased IL-13 level, mucus secretion, and gene expression of IL-33, Muc5ac, and Muc5b; compared to the non-treated asthma group. Azithromycin 15-27 interleukin 13 Mus musculus 52-57 35490266-8 2022 Treatment with azithromycin significantly decreased IL-13 level, mucus secretion, and gene expression of IL-33, Muc5ac, and Muc5b; compared to the non-treated asthma group. Azithromycin 15-27 interleukin 33 Mus musculus 105-110 35490266-8 2022 Treatment with azithromycin significantly decreased IL-13 level, mucus secretion, and gene expression of IL-33, Muc5ac, and Muc5b; compared to the non-treated asthma group. Azithromycin 15-27 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 112-118 35490266-8 2022 Treatment with azithromycin significantly decreased IL-13 level, mucus secretion, and gene expression of IL-33, Muc5ac, and Muc5b; compared to the non-treated asthma group. Azithromycin 15-27 mucin 5, subtype B, tracheobronchial Mus musculus 124-129 35336941-7 2022 However, in the severe patients of the second wave, iNOS levels were significantly lower in patients treated with steroids or azithromycin before the hospitalization, as compared to the untreated patients. Azithromycin 126-138 nitric oxide synthase 2 Homo sapiens 52-56 35341154-10 2022 Despite an additive effect against NO, KM plus AZM at an equal dose could synergistically suppress overrelease of the inflammatory cytokines TNF-alpha and IL-6 by LPS-induced RAW 264.7 cells. Azithromycin 47-50 tumor necrosis factor Mus musculus 141-150 35341154-10 2022 Despite an additive effect against NO, KM plus AZM at an equal dose could synergistically suppress overrelease of the inflammatory cytokines TNF-alpha and IL-6 by LPS-induced RAW 264.7 cells. Azithromycin 47-50 interleukin 6 Mus musculus 155-159 35107380-14 2022 Two hit drugs (azithromycin and ritonavir) strongly inhibited HEV production in culture supernatants, as well as intracellular expression of ORF2 protein, and may therefore be candidate novel anti-HEV drugs. Azithromycin 15-27 capsid protein Orthohepevirus A 141-145 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 interleukin 13 Homo sapiens 75-80 35193669-7 2022 Gene expression analysis showed upregulation of icsA in serotype 4a after exposure with azithromycin, whereas other genes in the VirF pathway were downregulated, and downregulation of virB in serotypes 2a and 3a after exposure with ciprofloxacin, while upregulation of noted genes was detected. Azithromycin 88-100 VirF Shigella flexneri 129-133 35215332-7 2022 Mechanistic insights underlying the synergistic effects of AZM and HCQ on iPSC-CM functionality are provided based on increased cellular accumulation of HCQ and AZM as well as increased Cx43- and Nav1.5-protein levels. Azithromycin 59-62 gap junction protein alpha 1 Homo sapiens 186-190 35215332-7 2022 Mechanistic insights underlying the synergistic effects of AZM and HCQ on iPSC-CM functionality are provided based on increased cellular accumulation of HCQ and AZM as well as increased Cx43- and Nav1.5-protein levels. Azithromycin 59-62 sodium voltage-gated channel alpha subunit 5 Homo sapiens 196-202 35159037-4 2022 Advanced macrolides, such as azithromycin, reduce the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K), a downstream mammalian target of rapamycin (mTOR) effector, and suppress the proliferation of T-cells. Azithromycin 29-41 ribosomal protein S6 kinase B1 Homo sapiens 73-104 35159037-4 2022 Advanced macrolides, such as azithromycin, reduce the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K), a downstream mammalian target of rapamycin (mTOR) effector, and suppress the proliferation of T-cells. Azithromycin 29-41 ribosomal protein S6 kinase B1 Homo sapiens 106-112 35159037-4 2022 Advanced macrolides, such as azithromycin, reduce the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K), a downstream mammalian target of rapamycin (mTOR) effector, and suppress the proliferation of T-cells. Azithromycin 29-41 mechanistic target of rapamycin kinase Homo sapiens 128-157 35159037-4 2022 Advanced macrolides, such as azithromycin, reduce the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K), a downstream mammalian target of rapamycin (mTOR) effector, and suppress the proliferation of T-cells. Azithromycin 29-41 mechanistic target of rapamycin kinase Homo sapiens 159-163 35072213-5 2022 Phytohaemagglutinin-induced release of pro-inflammatory mediators from PBMCs and production of intracellular cytokines by CD4+ and CD8+ T cells stimulated with phorbol 12-myristate 13-acetate and ionomycin in the presence or absence of 10 mug/mL azithromycin and 10 nM budesonide were determined using enzyme linked immunosorbent assay and flow cytometry. Azithromycin 246-258 CD4 molecule Homo sapiens 122-125 35072213-5 2022 Phytohaemagglutinin-induced release of pro-inflammatory mediators from PBMCs and production of intracellular cytokines by CD4+ and CD8+ T cells stimulated with phorbol 12-myristate 13-acetate and ionomycin in the presence or absence of 10 mug/mL azithromycin and 10 nM budesonide were determined using enzyme linked immunosorbent assay and flow cytometry. Azithromycin 246-258 CD8a molecule Homo sapiens 131-134 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 thymic stromal lymphopoietin Homo sapiens 167-171 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 macrophage migration inhibitory factor Homo sapiens 174-212 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 macrophage migration inhibitory factor Homo sapiens 214-217 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 CD4 molecule Homo sapiens 347-350 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 CD8a molecule Homo sapiens 356-359 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 interleukin 4 Homo sapiens 49-67 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 interleukin 5 Homo sapiens 69-73 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 interleukin 17A Homo sapiens 86-92 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 interleukin 4 Homo sapiens 134-138 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 C-X-C motif chemokine ligand 8 Homo sapiens 143-147 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 CD4 molecule Homo sapiens 151-154 35072213-6 2022 RESULTS: Azithromycin decreased the secretion of interleukin (IL) 4, IL-5, IL-13, and IL-17A from PBMCs, as well as the production of IL-4 and IL-8 by CD4+ and CD8+ T cells. Azithromycin 9-21 CD8a molecule Homo sapiens 160-163 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 interleukin 4 Homo sapiens 97-101 2844210-2 1988 The efficacy of an investigational macrolide, azithromycin, in the treatment of acute otitis media consequent to an infection by a strain of beta-lactamase-producing Haemophilus influenzae, was evaluated using the chinchilla animal model. Azithromycin 46-58 beta-lactamase TEM-1 Haemophilus influenzae 141-155 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 interleukin 5 Homo sapiens 103-107 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 C-X-C motif chemokine ligand 8 Homo sapiens 109-113 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 interleukin 13 Homo sapiens 115-120 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 interleukin 17A Homo sapiens 122-128 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 interleukin 33 Homo sapiens 130-135 35072213-7 2022 The combination of azithromycin and budesonide suppressed inflammatory response by inhibition of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF) release from PBMCs and by reduction of the percentage of IL-4-, IL-8-, interferon gamma- and tumor necrosis factor a-expressing CD4+ and CD8+ T cells. Azithromycin 19-31 thymic stromal lymphopoietin Homo sapiens 137-165 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 interleukin 4 Homo sapiens 66-70 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 interleukin 5 Homo sapiens 72-76 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 C-X-C motif chemokine ligand 8 Homo sapiens 78-82 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 interleukin 17A Homo sapiens 84-90 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 thymic stromal lymphopoietin Homo sapiens 92-96 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 interleukin 4 Homo sapiens 129-133 35072213-8 2022 The inhibitory effect of azithromycin combined with budesonide on IL-4, IL-5, IL-8, IL-17A, TSLP production by PBMCs, as well as IL-4 and IL-8 production by T helper cells and cytotoxic T lymphocytes was significantly greater than the effect of budesonide alone. Azithromycin 25-37 C-X-C motif chemokine ligand 8 Homo sapiens 138-142 35058480-2 2022 In particular, while recent studies examined COVID-19 associated arrhythmic risks from cardiac injury and/or from pharmacotherapy such as the combination of azithromycin (AZM) and hydroxychloroquine (HCQ), the role of IL-6 per se in increasing the arrhythmic risk remains poorly understood. Azithromycin 157-169 interleukin-6 Cavia porcellus 218-222 35058480-2 2022 In particular, while recent studies examined COVID-19 associated arrhythmic risks from cardiac injury and/or from pharmacotherapy such as the combination of azithromycin (AZM) and hydroxychloroquine (HCQ), the role of IL-6 per se in increasing the arrhythmic risk remains poorly understood. Azithromycin 171-174 interleukin-6 Cavia porcellus 218-222 33987628-7 2021 Azithromycin is a macrodial antibiotic working via the ABCB1 gene pathway. Azithromycin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 55-60 2847507-6 1988 Further, erythromycin A and azithromycin at concentrations of 10(-7) M, 10(-6) M and 10(-5) M significantly (p less than 0.01) reduced excocytosis of both lysosomal enzymes, beta-Gluc and beta-Glm from human PMNL initiated by BSA/anti-BSA in a dose-related fashion. Azithromycin 28-40 glucuronidase, beta Rattus norvegicus 174-183 2847507-7 1988 However, azithromycin was by far more effective (p less than 0.01) in decreasing extracellular release of beta-Gluc and beta-Glm either in the in vivo or in vitro experiments in comparison with erythromycin A. Azithromycin 9-21 glucuronidase, beta Rattus norvegicus 106-115 33753950-0 2021 Binding and drug displacement study of colchicine and bovine serum albumin in presence of azithromycin using multispectroscopic techniques and molecular dynamic simulation. Azithromycin 90-102 albumin Homo sapiens 61-74 33753950-1 2021 The binding and displacement interaction of colchicine and azithromycin to the model transport protein bovine serum albumin (BSA) was evaluated in this study. Azithromycin 59-71 albumin Homo sapiens 110-123 33704868-10 2021 CONCLUSION: Since reduced CD4 counts are associated with NTM, and cost and morbidity are high, azithromycin prophylaxis for CD4 count <200 cells/microl in high-risk patients should be considered. Azithromycin 95-107 CD4 molecule Homo sapiens 124-127 33277702-0 2021 Statin-induced rhabdomyolysis from azithromycin interaction in a patient with heterozygous SLCO1B1 polymorphism. Azithromycin 35-47 solute carrier organic anion transporter family member 1B1 Homo sapiens 91-98 33277702-3 2021 CASE DESCRIPTION: We report a case of simvastatin-induced rhabdomyolysis caused by an azithromycin drug interaction in a patient with heterozygous SLCO1B1 loss-of-function polymorphism. Azithromycin 86-98 solute carrier organic anion transporter family member 1B1 Homo sapiens 147-154 33277702-5 2021 Azithromycin mildly inhibits simvastatin"s CYP 3A4 hepatic metabolism, and the SLCO1B1 polymorphism reduces simvastatin hepatic uptake. Azithromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-50 33674391-5 2021 Here we study the effects of chloroquine, hydroxychloroquine, azithromycin, and remdesivir on hERG channels. Azithromycin 62-74 ETS transcription factor ERG Homo sapiens 94-98 34051014-6 2021 This enhanced cell death was dependent on wild-type-p53 status and autophagosome forming ability because TP53 knockout (KO) and ATG5-KO cells attenuated AZM-enhanced cytotoxicity. Azithromycin 153-156 tumor protein p53 Homo sapiens 105-109 34051014-6 2021 This enhanced cell death was dependent on wild-type-p53 status and autophagosome forming ability because TP53 knockout (KO) and ATG5-KO cells attenuated AZM-enhanced cytotoxicity. Azithromycin 153-156 autophagy related 5 Homo sapiens 128-132 32804426-0 2021 Possible role of ABCB1 in lysosomal accumulation of azithromycin in COVID-19 therapy. Azithromycin 52-64 ATP binding cassette subfamily B member 1 Homo sapiens 17-22 33674391-10 2021 Significance Statement This work demonstrates that among off-label potential COVID-19 treatment drugs chloroquine, hydroxychloroquine, azithromycin, and remdesivir, the former two drugs block hERG potassium channels while the latter two drugs do not. Azithromycin 135-147 ETS transcription factor ERG Homo sapiens 192-196 33937285-5 2021 Among such class of drugs, azithromycin is described as azalide and is well-known for its ability to decrease the production of pro-inflammatory cytokines, including matrix metalloproteinases, tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8. Azithromycin 27-39 tumor necrosis factor Homo sapiens 193-220 33953352-4 2021 Our findings demonstrate a strong relationship between Kallikrein Related Peptidase 6 (KLK6) mutation status and the ability of azithromycin to kill cancer cells in vitro. Azithromycin 128-140 kallikrein related peptidase 6 Homo sapiens 55-85 33953352-4 2021 Our findings demonstrate a strong relationship between Kallikrein Related Peptidase 6 (KLK6) mutation status and the ability of azithromycin to kill cancer cells in vitro. Azithromycin 128-140 kallikrein related peptidase 6 Homo sapiens 87-91 33685581-2 2021 Anecdotally, low rectal pH could reduce rectal azithromycin concentrations, with in vitro studies reporting higher minimum inhibitory concentrations (MICs) with lower pHs for antibiotics used to treat sexually transmissible infections (STIs). Azithromycin 47-59 phenylalanine hydroxylase Homo sapiens 24-26 33685581-10 2021 And 50% had a rectal pH <8.0, with 27% reporting a pH between 6.0 and 6.5 where treatment failure is thought to occur for azithromycin. Azithromycin 122-134 phenylalanine hydroxylase Homo sapiens 51-53 33685581-12 2021 CONCLUSIONS: Lower rectal pH among MSM is associated with older age and could influence the rectal pharmacokinetics of azithromycin and other drugs influenced by pH and may therefore affect treatment outcomes. Azithromycin 119-131 phenylalanine hydroxylase Homo sapiens 26-28 33685581-12 2021 CONCLUSIONS: Lower rectal pH among MSM is associated with older age and could influence the rectal pharmacokinetics of azithromycin and other drugs influenced by pH and may therefore affect treatment outcomes. Azithromycin 119-131 phenylalanine hydroxylase Homo sapiens 162-164 33937285-5 2021 Among such class of drugs, azithromycin is described as azalide and is well-known for its ability to decrease the production of pro-inflammatory cytokines, including matrix metalloproteinases, tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8. Azithromycin 27-39 interleukin 6 Homo sapiens 222-240 33937285-5 2021 Among such class of drugs, azithromycin is described as azalide and is well-known for its ability to decrease the production of pro-inflammatory cytokines, including matrix metalloproteinases, tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8. Azithromycin 27-39 C-X-C motif chemokine ligand 8 Homo sapiens 246-250 32969125-8 2021 Of relevance to severe coronavirus-19 disease (COVID-19), which is characterised by an over-exuberant innate inflammatory response, AZM also has anti-inflammatory properties including suppression of IL-1beta, IL-2, TNF and GM-CSF. Azithromycin 132-135 interleukin 1 alpha Homo sapiens 199-207 33894712-10 2021 A negative correlation was observed between AZM concentration in lung tissue and interleukin-6 (IL-6) expression. Azithromycin 44-47 interleukin 6 Homo sapiens 81-94 33894712-10 2021 A negative correlation was observed between AZM concentration in lung tissue and interleukin-6 (IL-6) expression. Azithromycin 44-47 interleukin 6 Homo sapiens 96-100 33607534-8 2021 RESULTS: AZT treatment alone inhibited cell viability, induced apoptosis and enhanced caspase 3/7 activity in both K562S and high MDR-1 (Pgp) expressing K562R cells. Azithromycin 9-12 caspase 3 Homo sapiens 86-97 33607534-8 2021 RESULTS: AZT treatment alone inhibited cell viability, induced apoptosis and enhanced caspase 3/7 activity in both K562S and high MDR-1 (Pgp) expressing K562R cells. Azithromycin 9-12 ATP binding cassette subfamily B member 1 Homo sapiens 130-135 33607534-8 2021 RESULTS: AZT treatment alone inhibited cell viability, induced apoptosis and enhanced caspase 3/7 activity in both K562S and high MDR-1 (Pgp) expressing K562R cells. Azithromycin 9-12 ATP binding cassette subfamily B member 1 Homo sapiens 137-140 33607534-9 2021 Moreover, combination of AZT/IMA suppressed cell viability, induced apoptosis and caspase3/7 activity more effectively and significantly compared to K562R cells treated with only IMA or AZT. Azithromycin 25-28 caspase 3 Homo sapiens 82-92 33607534-10 2021 Furthermore, AZT and AZT/IMA combination decreased Pgp function in K562R cells in comparison with their controls. Azithromycin 13-16 ATP binding cassette subfamily B member 1 Homo sapiens 51-54 33607534-10 2021 Furthermore, AZT and AZT/IMA combination decreased Pgp function in K562R cells in comparison with their controls. Azithromycin 21-24 ATP binding cassette subfamily B member 1 Homo sapiens 51-54 33607534-11 2021 Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells. Azithromycin 30-33 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 33607534-11 2021 Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells. Azithromycin 30-33 BCL2 apoptosis regulator Homo sapiens 82-87 33607534-11 2021 Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells. Azithromycin 47-50 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 33607534-11 2021 Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells. Azithromycin 47-50 BCL2 apoptosis regulator Homo sapiens 82-87 33607534-13 2021 One of the mechanisms underlying the potent anticancer effect of combined AZT/IMA could be its ability to inhibit Pgp function and increase intracellular accumulation of IMA which leads to the induction of apoptosis in K562R cells. Azithromycin 74-77 ATP binding cassette subfamily B member 1 Homo sapiens 114-117 33655586-0 2021 Azithromycin inhibited oxidative stress and apoptosis of high glucose-induced podocytes by inhibiting STAT1 pathway. Azithromycin 0-12 signal transducer and activator of transcription 1 Homo sapiens 102-107 33655586-12 2021 AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase-3, 6, 9, and promote the expression of Bcl-2 (p < .001). Azithromycin 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 48-51 33655586-12 2021 AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase-3, 6, 9, and promote the expression of Bcl-2 (p < .001). Azithromycin 0-3 BCL2 apoptosis regulator Homo sapiens 111-116 33655586-13 2021 Furthermore, the expression of STAT1 was increased after high glucose induction, while the expression of STAT1 was decreased after AZM action (p < .01). Azithromycin 131-134 signal transducer and activator of transcription 1 Homo sapiens 105-110 33655586-14 2021 By adding a STAT1 agonist IFN-gamma, the effects of AZM on inflammation, oxidative stress, and apoptosis of high glucose-induced podocytes were inhibited (p < .05). Azithromycin 52-55 signal transducer and activator of transcription 1 Homo sapiens 12-17 33655586-14 2021 By adding a STAT1 agonist IFN-gamma, the effects of AZM on inflammation, oxidative stress, and apoptosis of high glucose-induced podocytes were inhibited (p < .05). Azithromycin 52-55 interferon gamma Homo sapiens 26-35 33655586-15 2021 AZM inhibited inflammation, oxidative stress, and apoptosis of high glucose-induced podocytes by inhibiting STAT1 pathway. Azithromycin 0-3 signal transducer and activator of transcription 1 Homo sapiens 108-113 32969125-8 2021 Of relevance to severe coronavirus-19 disease (COVID-19), which is characterised by an over-exuberant innate inflammatory response, AZM also has anti-inflammatory properties including suppression of IL-1beta, IL-2, TNF and GM-CSF. Azithromycin 132-135 interleukin 2 Homo sapiens 209-213 32969125-8 2021 Of relevance to severe coronavirus-19 disease (COVID-19), which is characterised by an over-exuberant innate inflammatory response, AZM also has anti-inflammatory properties including suppression of IL-1beta, IL-2, TNF and GM-CSF. Azithromycin 132-135 tumor necrosis factor Homo sapiens 215-218 32969125-8 2021 Of relevance to severe coronavirus-19 disease (COVID-19), which is characterised by an over-exuberant innate inflammatory response, AZM also has anti-inflammatory properties including suppression of IL-1beta, IL-2, TNF and GM-CSF. Azithromycin 132-135 colony stimulating factor 2 Homo sapiens 223-229 32969125-9 2021 AZM inhibits T cells by inhibiting calcineurin signalling, mammalian target of rapamycin activity and NFkappaB activation. Azithromycin 0-3 mechanistic target of rapamycin kinase Homo sapiens 59-88 33569770-0 2021 Sputum TNF markers are increased in neutrophilic and severe asthma andarereduced by azithromycin treatment. Azithromycin 84-96 tumor necrosis factor Homo sapiens 7-10 33345848-0 2021 Off-label use of chloroquine, hydroxychloroquine, azithromycin and lopinavir/ritonavir in COVID-19 risks prolonging the QT interval by targeting the hERG channel. Azithromycin 50-62 ETS transcription factor ERG Homo sapiens 149-153 33345848-3 2021 Clinically, however, many drugs, including those currently used in COVID-19, such as chloroquine, hydroxychloroquine, azithromycin, and lopinavir/ritonavir, may cause cardiotoxicity by acting on cardiac potassium channels and the hERG channel through their off-target effects. Azithromycin 118-130 ETS transcription factor ERG Homo sapiens 230-234 33609487-16 2021 Treatment with low dose azithromycin was associated with a significant reduction in NETs in sputum over 12 months in both bronchiectasis and asthma. Azithromycin 24-36 serine peptidase inhibitor Kazal type 5 Homo sapiens 84-88 33569770-2 2021 Dysregulation of the inflammatory tumour necrosis factor(TNF) pathwayis implicated in asthma and could be suppressed by azithromycin.We aimed to determine the inflammatory and clinical associations of soluble TNF signalling proteins (TNFreceptors [TNFR] 1 and 2, TNF)in sputum and serum, and to test the effect of 48 weeks of azithromycin vs placebo on TNF markers. Azithromycin 120-132 tumor necrosis factor Homo sapiens 57-60 33569770-2 2021 Dysregulation of the inflammatory tumour necrosis factor(TNF) pathwayis implicated in asthma and could be suppressed by azithromycin.We aimed to determine the inflammatory and clinical associations of soluble TNF signalling proteins (TNFreceptors [TNFR] 1 and 2, TNF)in sputum and serum, and to test the effect of 48 weeks of azithromycin vs placebo on TNF markers. Azithromycin 120-132 tumor necrosis factor Homo sapiens 209-212 33569770-2 2021 Dysregulation of the inflammatory tumour necrosis factor(TNF) pathwayis implicated in asthma and could be suppressed by azithromycin.We aimed to determine the inflammatory and clinical associations of soluble TNF signalling proteins (TNFreceptors [TNFR] 1 and 2, TNF)in sputum and serum, and to test the effect of 48 weeks of azithromycin vs placebo on TNF markers. Azithromycin 120-132 tumor necrosis factor Homo sapiens 209-212 33569770-2 2021 Dysregulation of the inflammatory tumour necrosis factor(TNF) pathwayis implicated in asthma and could be suppressed by azithromycin.We aimed to determine the inflammatory and clinical associations of soluble TNF signalling proteins (TNFreceptors [TNFR] 1 and 2, TNF)in sputum and serum, and to test the effect of 48 weeks of azithromycin vs placebo on TNF markers. Azithromycin 120-132 tumor necrosis factor Homo sapiens 209-212 33569770-2 2021 Dysregulation of the inflammatory tumour necrosis factor(TNF) pathwayis implicated in asthma and could be suppressed by azithromycin.We aimed to determine the inflammatory and clinical associations of soluble TNF signalling proteins (TNFreceptors [TNFR] 1 and 2, TNF)in sputum and serum, and to test the effect of 48 weeks of azithromycin vs placebo on TNF markers. Azithromycin 326-338 tumor necrosis factor Homo sapiens 57-60 33569770-7 2021 Sputum and serum TNFR2 were increased in frequentexacerbators.Azithromycin treatmentsignificantly reducedsputum TNFR2 and TNFrelative to placebo, specifically in non-eosinophilic participants. Azithromycin 62-74 TNF receptor superfamily member 1B Homo sapiens 17-22 33569770-7 2021 Sputum and serum TNFR2 were increased in frequentexacerbators.Azithromycin treatmentsignificantly reducedsputum TNFR2 and TNFrelative to placebo, specifically in non-eosinophilic participants. Azithromycin 62-74 TNF receptor superfamily member 1B Homo sapiens 112-117 33569770-9 2021 Suppression of dysregulated TNF signalling by azithromycin could contribute to its therapeutic mechanism. Azithromycin 46-58 tumor necrosis factor Homo sapiens 28-31 33628506-14 2021 The administration of azithromycin to the Control group increased CRP and IL-6 levels, while reduced IL-10 and TNF-alpha on day 7 (p < 0.0001) compared with day 1. Azithromycin 22-34 C-reactive protein Homo sapiens 66-69 33628506-14 2021 The administration of azithromycin to the Control group increased CRP and IL-6 levels, while reduced IL-10 and TNF-alpha on day 7 (p < 0.0001) compared with day 1. Azithromycin 22-34 interleukin 6 Homo sapiens 74-78 33628506-14 2021 The administration of azithromycin to the Control group increased CRP and IL-6 levels, while reduced IL-10 and TNF-alpha on day 7 (p < 0.0001) compared with day 1. Azithromycin 22-34 interleukin 10 Homo sapiens 101-106 33628506-14 2021 The administration of azithromycin to the Control group increased CRP and IL-6 levels, while reduced IL-10 and TNF-alpha on day 7 (p < 0.0001) compared with day 1. Azithromycin 22-34 tumor necrosis factor Homo sapiens 111-120 33336605-9 2021 When cells were pretreated with azithromycin and exposed to 5% CSE for 3 h, there was a significant dose-dependent decrease in the expression of IL-6 mRNA. Azithromycin 32-44 interleukin 6 Homo sapiens 145-149 33336605-10 2021 A final concentration of 9 microg/mL of azithromycin was sufficient to decrease IL-6, IL-8 mRNA, and extracellular IL-8 levels. Azithromycin 40-52 C-X-C motif chemokine ligand 8 Homo sapiens 86-90 33336605-10 2021 A final concentration of 9 microg/mL of azithromycin was sufficient to decrease IL-6, IL-8 mRNA, and extracellular IL-8 levels. Azithromycin 40-52 interleukin 6 Homo sapiens 80-84 33336605-10 2021 A final concentration of 9 microg/mL of azithromycin was sufficient to decrease IL-6, IL-8 mRNA, and extracellular IL-8 levels. Azithromycin 40-52 C-X-C motif chemokine ligand 8 Homo sapiens 115-119 33550966-2 2021 The present work is an effort for a computational target to block the spike proteins (S) and ACE2 receptor proteins with Macrolide antibiotics like Azithromycin, (AZM), Clarithromycin (CLAM) and Erythromycin (ERY) along with RNA-dependent RNA polymerase (RdRp). Azithromycin 148-160 angiotensin converting enzyme 2 Homo sapiens 93-97 33336605-11 2021 Conclusion: Pretreatment with azithromycin decreased the expression of IL-6 and IL-8 mRNA and the release of IL-8 in bronchial epithelial cells exposed to cigarette smoke. Azithromycin 30-42 interleukin 6 Homo sapiens 71-75 33336605-11 2021 Conclusion: Pretreatment with azithromycin decreased the expression of IL-6 and IL-8 mRNA and the release of IL-8 in bronchial epithelial cells exposed to cigarette smoke. Azithromycin 30-42 C-X-C motif chemokine ligand 8 Homo sapiens 80-84 33336605-11 2021 Conclusion: Pretreatment with azithromycin decreased the expression of IL-6 and IL-8 mRNA and the release of IL-8 in bronchial epithelial cells exposed to cigarette smoke. Azithromycin 30-42 C-X-C motif chemokine ligand 8 Homo sapiens 109-113 32725797-0 2021 Azithromycin and ciprofloxacin inhibit interleukin-8 secretion without disrupting human sinonasal epithelial integrity in vitro. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Homo sapiens 39-52 33211371-9 2021 Using a NPC1-pHluorin2 reporter cell line, we confirmed that AZ treatment could alkalize the vesicles containing IAV virions, thereby preventing pH-dependent membrane fusion. Azithromycin 61-63 NPC intracellular cholesterol transporter 1 Homo sapiens 8-12 33616621-8 2021 Smo antagonist, cyclopamine, reduced cell numbers, and the expression of Ki67 in MGECM, and promoted the expression of SREBP1 and lipid production in DM + AZM. Azithromycin 155-158 smoothened, frizzled class receptor Rattus norvegicus 0-3 33616621-8 2021 Smo antagonist, cyclopamine, reduced cell numbers, and the expression of Ki67 in MGECM, and promoted the expression of SREBP1 and lipid production in DM + AZM. Azithromycin 155-158 sterol regulatory element binding transcription factor 1 Rattus norvegicus 119-125 33616621-9 2021 Smo agonist, SAG, inhibited the expression of SREBP1 and lipid accumulation in DM + AZM but showed no significant effects on raising cell numbers and the expression of Ki67 in MGECM. Azithromycin 84-87 smoothened, frizzled class receptor Rattus norvegicus 0-3 33616621-9 2021 Smo agonist, SAG, inhibited the expression of SREBP1 and lipid accumulation in DM + AZM but showed no significant effects on raising cell numbers and the expression of Ki67 in MGECM. Azithromycin 84-87 sterol regulatory element binding transcription factor 1 Rattus norvegicus 46-52 33414242-2 2021 In a predefined substudy of the original AMAZES protocol (500 mg, three times a week for 48 weeks), we report that AZM treatment reduces key sputum inflammatory proteins (interleukin (IL)-6, IL-1beta and extracellular DNA), which is more evident in non-eosinophilic asthma (NEA). Azithromycin 115-118 interleukin 6 Homo sapiens 171-189 33414242-2 2021 In a predefined substudy of the original AMAZES protocol (500 mg, three times a week for 48 weeks), we report that AZM treatment reduces key sputum inflammatory proteins (interleukin (IL)-6, IL-1beta and extracellular DNA), which is more evident in non-eosinophilic asthma (NEA). Azithromycin 115-118 interleukin 1 alpha Homo sapiens 191-199 33414432-2 2021 Here, we report that lysosomotropic agents, including azithromycin, chloroquine, and hydroxychloroquine, can trigger eIF2alpha phosphorylation in vitro (in cultured human cells) and, as validated for hydroxychloroquine, in vivo (in mice). Azithromycin 54-66 eukaryotic translation initiation factor 2A Homo sapiens 117-126 33550966-2 2021 The present work is an effort for a computational target to block the spike proteins (S) and ACE2 receptor proteins with Macrolide antibiotics like Azithromycin, (AZM), Clarithromycin (CLAM) and Erythromycin (ERY) along with RNA-dependent RNA polymerase (RdRp). Azithromycin 163-166 angiotensin converting enzyme 2 Homo sapiens 93-97 33396644-7 2020 In response to LPS stimulation, the gene expression levels of IL-6 and IL-8 in hGFs increased due to AZM in a concentration-dependent manner, and phosphorylation of nuclear factor kappa B (NF-kappaB) was also promoted. Azithromycin 101-104 interleukin 6 Homo sapiens 62-66 33396644-7 2020 In response to LPS stimulation, the gene expression levels of IL-6 and IL-8 in hGFs increased due to AZM in a concentration-dependent manner, and phosphorylation of nuclear factor kappa B (NF-kappaB) was also promoted. Azithromycin 101-104 C-X-C motif chemokine ligand 8 Homo sapiens 71-75 33396644-8 2020 Additionally, AZM caused an increase in MMP-1 expression in hGFs, whereas it did not affect the expression of any of the analyzed genes in hPLFs. Azithromycin 14-17 matrix metallopeptidase 1 Homo sapiens 40-45 33396644-10 2020 Thus, AZM may increase the expression of IL-6 and IL-8 under LPS stimulation to modify the inflammatory response and increase the expression of MMP-1 to promote connective tissue remodeling. Azithromycin 6-9 interleukin 6 Homo sapiens 41-45 33396644-10 2020 Thus, AZM may increase the expression of IL-6 and IL-8 under LPS stimulation to modify the inflammatory response and increase the expression of MMP-1 to promote connective tissue remodeling. Azithromycin 6-9 C-X-C motif chemokine ligand 8 Homo sapiens 50-54 33396644-10 2020 Thus, AZM may increase the expression of IL-6 and IL-8 under LPS stimulation to modify the inflammatory response and increase the expression of MMP-1 to promote connective tissue remodeling. Azithromycin 6-9 matrix metallopeptidase 1 Homo sapiens 144-149 33179586-6 2022 We have also performed docking of drugs Lopinavir, Ribavirin, and Azithromycin on SARS-CoV-2 Mpro. Azithromycin 66-78 NEWENTRY Severe acute respiratory syndrome-related coronavirus 93-97 32436162-6 2020 RESULTS: LPS and TNF-alpha induced a similar pattern of IL-1beta mRNA expression, with peak expression at 1 h. For most mediators, gene expression in neutrophils activated by LPS was markedly reduced in a dose-dependent manner by AZM. Azithromycin 230-233 tumor necrosis factor Homo sapiens 17-26 33002511-1 2020 Previous research demonstrates that, in clinically relevant concentrations, azithromycin can boost the ability of RNA viruses to induce type 1 interferon by amplifying the expression and virally-mediated activation of MDA5. Azithromycin 76-88 interferon induced with helicase C domain 1 Homo sapiens 218-222 33077651-5 2020 Overall, azithromycin-SPR-741 (MIC90, 2-4 mg/L) and minocycline-SPR-741 (MIC90, 0.5-2 mg/L) showed the lowest MIC90 against different subsets of E. coli isolates, except for azithromycin-SPR-741 (MIC90, 16 mg/L) against the AmpC and metallo-beta-lactamase subsets. Azithromycin 9-21 beta-lactamase Escherichia coli 224-228 33098839-7 2020 The best core hub protein drug targets involved in QT interval prolongation were identified as HSP90AA1 exclusively associated with HCQ, while AKT1 exclusively associated with AZM on the basis of node degree value. Azithromycin 176-179 AKT serine/threonine kinase 1 Homo sapiens 143-147 33098839-8 2020 It was found that PI3K/Akt, VEGF, ERBB2 pathways must be given consideration for understanding the role of HCQ and AZM in QT interval prolongation. Azithromycin 115-118 erb-b2 receptor tyrosine kinase 2 Homo sapiens 34-39 32967779-5 2020 The observed differences were associated with different inhibitory/inactivation potentials of troleandomycin, erythromycin, clarithromycin and azithromycin, suggesting CYP3A4 Template also as a tool for drug-interaction mechanisms. Azithromycin 143-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 33173988-2 2020 We previously reported that macrolide antibiotics such as azithromycin (AZM) and clarithromycin (CAM) potently inhibit autophagic flux and that combining AZM or CAM with the epidermal growth factor receptor inhibitors enhanced their antitumor effect against various cancer cells. Azithromycin 58-70 epidermal growth factor receptor Homo sapiens 174-206 33173988-2 2020 We previously reported that macrolide antibiotics such as azithromycin (AZM) and clarithromycin (CAM) potently inhibit autophagic flux and that combining AZM or CAM with the epidermal growth factor receptor inhibitors enhanced their antitumor effect against various cancer cells. Azithromycin 72-75 epidermal growth factor receptor Homo sapiens 174-206 33173988-2 2020 We previously reported that macrolide antibiotics such as azithromycin (AZM) and clarithromycin (CAM) potently inhibit autophagic flux and that combining AZM or CAM with the epidermal growth factor receptor inhibitors enhanced their antitumor effect against various cancer cells. Azithromycin 154-157 epidermal growth factor receptor Homo sapiens 174-206 33173988-7 2020 Furthermore, the A549 cell line with ATG5 knockout exhibited complete inhibition of autophagosome formation, which did not affect LPZ + AZM treatment-induced cytotoxicity, thus excluding the involvement of autophagy-dependent cell death in LPZ + AZM treatment-induced cell death. Azithromycin 246-249 autophagy related 5 Homo sapiens 37-41 33173988-9 2020 Notably, lysosomal galectin-3 puncta expression induced due to lysosomal membrane permeabilization was increased in cells treated with LPZ + AZM combination as compared to the treatment by either agent alone. Azithromycin 141-144 galectin 3 Homo sapiens 19-29 33150590-8 2021 Low levels of TNF-alpha and IL-10 and high levels of CCL22 predicted better treatment response to azithromycin (p-values < 0.05). Azithromycin 98-110 C-C motif chemokine ligand 22 Homo sapiens 53-58 33150590-9 2021 CONCLUSION: Upper airway immune mediator levels were altered during episodes of asthma-like symptoms, and levels of TNF-alpha, CCL22 and IL-10 may predict the response to azithromycin treatment. Azithromycin 171-183 tumor necrosis factor Homo sapiens 116-125 33150590-9 2021 CONCLUSION: Upper airway immune mediator levels were altered during episodes of asthma-like symptoms, and levels of TNF-alpha, CCL22 and IL-10 may predict the response to azithromycin treatment. Azithromycin 171-183 C-C motif chemokine ligand 22 Homo sapiens 127-132 33150590-9 2021 CONCLUSION: Upper airway immune mediator levels were altered during episodes of asthma-like symptoms, and levels of TNF-alpha, CCL22 and IL-10 may predict the response to azithromycin treatment. Azithromycin 171-183 interleukin 10 Homo sapiens 137-142 33195812-9 2020 Conclusion: Annual mass treatment with azithromycin eye drops was shown to be effective in reducing TF to a level <=5% one year after a 3-round annual mass treatment in an endemic region at the district level. Azithromycin 39-51 coagulation factor III, tissue factor Homo sapiens 100-102 32857620-0 2020 Azithromycin Downregulates Gene Expression of IL-1beta and Pathways Involving TMPRSS2 and TMPRSS11D Required by SARS-CoV-2. Azithromycin 0-12 interleukin 1 alpha Homo sapiens 46-54 32857620-0 2020 Azithromycin Downregulates Gene Expression of IL-1beta and Pathways Involving TMPRSS2 and TMPRSS11D Required by SARS-CoV-2. Azithromycin 0-12 transmembrane serine protease 2 Homo sapiens 78-85 32857620-0 2020 Azithromycin Downregulates Gene Expression of IL-1beta and Pathways Involving TMPRSS2 and TMPRSS11D Required by SARS-CoV-2. Azithromycin 0-12 transmembrane serine protease 11D Homo sapiens 90-99 32857620-8 2020 RESULTS: Cell cultures treated with 10microg of azithromycin significantly downregulated receptor-mediated endocytosis canonical pathways involving TMPRSS2 and TMPRSS11D genes. Azithromycin 48-60 transmembrane serine protease 2 Homo sapiens 148-155 32857620-8 2020 RESULTS: Cell cultures treated with 10microg of azithromycin significantly downregulated receptor-mediated endocytosis canonical pathways involving TMPRSS2 and TMPRSS11D genes. Azithromycin 48-60 transmembrane serine protease 11D Homo sapiens 160-169 32857620-11 2020 CONCLUSIONS: This proof of concept demonstrates azithromycin downregulates pathways involving serine proteases TMPRSS2 and TMPRSS11D required for SARS-CoV-2 activation and its cell-to-cell transmission while downregulating pro-inflammatory cytokine IL-1beta, NDST-1 and their associated pathways. Azithromycin 48-60 transmembrane serine protease 2 Homo sapiens 111-118 32857620-11 2020 CONCLUSIONS: This proof of concept demonstrates azithromycin downregulates pathways involving serine proteases TMPRSS2 and TMPRSS11D required for SARS-CoV-2 activation and its cell-to-cell transmission while downregulating pro-inflammatory cytokine IL-1beta, NDST-1 and their associated pathways. Azithromycin 48-60 transmembrane serine protease 13 Homo sapiens 123-131 32857620-11 2020 CONCLUSIONS: This proof of concept demonstrates azithromycin downregulates pathways involving serine proteases TMPRSS2 and TMPRSS11D required for SARS-CoV-2 activation and its cell-to-cell transmission while downregulating pro-inflammatory cytokine IL-1beta, NDST-1 and their associated pathways. Azithromycin 48-60 interleukin 1 alpha Homo sapiens 249-257 32857620-11 2020 CONCLUSIONS: This proof of concept demonstrates azithromycin downregulates pathways involving serine proteases TMPRSS2 and TMPRSS11D required for SARS-CoV-2 activation and its cell-to-cell transmission while downregulating pro-inflammatory cytokine IL-1beta, NDST-1 and their associated pathways. Azithromycin 48-60 N-deacetylase and N-sulfotransferase 1 Homo sapiens 259-265 33117343-7 2020 Furthermore, AZM significantly inhibited the inflammatory cytokines IFN-gamma and IL-4 production, CCR4 and CXCR3 receptor expression, and viability of Th0, Th1-like, and Th2-like subsets. Azithromycin 13-16 interferon gamma Homo sapiens 68-77 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 C-C motif chemokine ligand 2 Homo sapiens 71-75 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 cathepsin B Homo sapiens 77-81 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 C-X-C motif chemokine ligand 8 Homo sapiens 83-88 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 interleukin 1 beta Homo sapiens 90-94 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 interleukin 6 Homo sapiens 96-99 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 tumor necrosis factor Homo sapiens 104-107 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 BCL2 like 1 Homo sapiens 178-184 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Azithromycin 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 32920000-7 2020 In contrast to lopinavir/ritonavir, chloroquine/hydroxychloroquine + azithromycin downregulated the expression of TNF and IL6. Azithromycin 69-81 tumor necrosis factor Homo sapiens 114-117 32920000-7 2020 In contrast to lopinavir/ritonavir, chloroquine/hydroxychloroquine + azithromycin downregulated the expression of TNF and IL6. Azithromycin 69-81 interleukin 6 Homo sapiens 122-125 32868325-10 2020 Azithromycin resistance was observed in four (15%) isolates (epidemiological cut-off); all with mutations in the mtrR promoter region. Azithromycin 0-12 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 113-117 32615080-0 2020 GR-C/EBPalpha-IGF1 axis mediated azithromycin-induced liver developmental toxicity in fetal mice. Azithromycin 33-45 insulin-like growth factor 1 Mus musculus 14-18 32615080-7 2020 Furthermore, azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPalpha signal and reducing the expression and secretion levels of IGF1 in HepG2 cells. Azithromycin 13-25 insulin like growth factor 1 Homo sapiens 188-192 32615080-9 2020 These results indicated that PAE could cause fetal liver developmental toxicity in mice, and one of the main mechanisms was that azithromycin activated the GR-C/EBPalpha signal, inhibited the IGF1 signal pathway, and then disturbed the hepatic proliferation, apoptosis, differentiation, and glycose and lipid metabolism. Azithromycin 129-141 insulin-like growth factor 1 Mus musculus 192-196 32905367-2 2020 The present study aimed to explore the clinical efficacy of azithromycin combined with doxycycline in patients with NGU and its effect on serum levels of inflammatory cytokine interleukin-6 (IL-6). Azithromycin 60-72 interleukin 6 Homo sapiens 176-189 32905367-2 2020 The present study aimed to explore the clinical efficacy of azithromycin combined with doxycycline in patients with NGU and its effect on serum levels of inflammatory cytokine interleukin-6 (IL-6). Azithromycin 60-72 interleukin 6 Homo sapiens 191-195 33037471-6 2020 This study highlights the impact of hydrophobic azithromycin enrichment on particle surface irrespective of the nozzle type, on the prevention of moisture-induced deterioration of FPF for hygroscopic colistin. Azithromycin 48-60 TNF receptor superfamily member 1A Homo sapiens 180-183 33312066-8 2020 Based on high alternative allele frequencies in population and the functional effect of the variants, ABCB1 rs1045642 and rs2032582 could be relevant for reduced clearance of azithromycin, lopinavir and ritonavir drugs and UGT1A7 rs17868323 for hyperbilirubinemia in ritonavir treated COVID-19 patients in Serbian population. Azithromycin 175-187 ATP binding cassette subfamily B member 1 Homo sapiens 102-107 33312066-8 2020 Based on high alternative allele frequencies in population and the functional effect of the variants, ABCB1 rs1045642 and rs2032582 could be relevant for reduced clearance of azithromycin, lopinavir and ritonavir drugs and UGT1A7 rs17868323 for hyperbilirubinemia in ritonavir treated COVID-19 patients in Serbian population. Azithromycin 175-187 UDP glucuronosyltransferase family 1 member A7 Homo sapiens 223-229 33117343-7 2020 Furthermore, AZM significantly inhibited the inflammatory cytokines IFN-gamma and IL-4 production, CCR4 and CXCR3 receptor expression, and viability of Th0, Th1-like, and Th2-like subsets. Azithromycin 13-16 interleukin 4 Homo sapiens 82-86 33117343-7 2020 Furthermore, AZM significantly inhibited the inflammatory cytokines IFN-gamma and IL-4 production, CCR4 and CXCR3 receptor expression, and viability of Th0, Th1-like, and Th2-like subsets. Azithromycin 13-16 C-C motif chemokine receptor 4 Homo sapiens 99-103 33117343-7 2020 Furthermore, AZM significantly inhibited the inflammatory cytokines IFN-gamma and IL-4 production, CCR4 and CXCR3 receptor expression, and viability of Th0, Th1-like, and Th2-like subsets. Azithromycin 13-16 C-X-C motif chemokine receptor 3 Homo sapiens 108-122 32738306-7 2020 The findings showed AZM affinity scores (DeltaG) with strong interactions with ACE2, CTSL, Mpro and RBD. Azithromycin 20-23 angiotensin converting enzyme 2 Homo sapiens 79-83 32668165-10 2020 Second, many CF patients are treated with azithromycin, which suppresses viral infection and lung inflammation and inhibits the activity of furin, a serine protease. Azithromycin 42-54 furin, paired basic amino acid cleaving enzyme Homo sapiens 140-145 32668165-10 2020 Second, many CF patients are treated with azithromycin, which suppresses viral infection and lung inflammation and inhibits the activity of furin, a serine protease. Azithromycin 42-54 coagulation factor II, thrombin Homo sapiens 149-164 32738306-7 2020 The findings showed AZM affinity scores (DeltaG) with strong interactions with ACE2, CTSL, Mpro and RBD. Azithromycin 20-23 cathepsin L Homo sapiens 85-89 32738306-7 2020 The findings showed AZM affinity scores (DeltaG) with strong interactions with ACE2, CTSL, Mpro and RBD. Azithromycin 20-23 NEWENTRY Severe acute respiratory syndrome-related coronavirus 91-95 32889431-0 2020 Deglycosylated Azithromycin Targets Transgelin to Enhance Intestinal Smooth Muscle Function. Azithromycin 15-27 transgelin Mus musculus 36-46 32811545-16 2020 Two strategies have been commonly implicated in gonococcal resistance against azithromycin: over expression of an efflux pump (due to mutations at mtrR coding region) and decreased antimicrobial affinity (due to mutations in genes encoding the 23S ribosomal subunit). Azithromycin 78-90 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 147-151 32763436-12 2020 AZM suppressed pathogen-stimulated NF-kappaB activation and cytokine production, whereas AMP, AMX, and CLI reduced only cytokine production moderately. Azithromycin 0-3 nuclear factor kappa B subunit 1 Homo sapiens 35-44 32782021-8 2020 Illumina and Nanopore sequencing and plasmid coverage analysis further confirmed that azithromycin-resistant strains carried a novel IncFII plasmid harboring mphA and blaTEM-1 resistance genes. Azithromycin 86-98 beta-lactamase Escherichia coli 167-175 32559772-3 2020 The aim of this study was to compare the effects of erythromycin, clarithromycin and azithromycin on cell viability and expression of ERG1 gene in H9c2 cells. Azithromycin 85-97 potassium voltage-gated channel subfamily H member 2 Rattus norvegicus 134-138 32559772-0 2020 Comparative Study of the Effect of Macrolide Antibiotics Erythromycin, Clarithromycin, and Azithromycin on the ERG1 Gene Expression in H9c2 Cardiomyoblast Cells. Azithromycin 91-103 potassium voltage-gated channel subfamily H member 2 Rattus norvegicus 111-115 32125889-0 2020 The effect of Gender and ABCB1 Gene Polymorphism on the Pharmacokinetics of Azithromycin in Healthy Male and Female Pakistani Subjects. Azithromycin 76-88 ATP binding cassette subfamily B member 1 Homo sapiens 25-30 32125889-1 2020 BACKGROUND: In the current study, the possible outcome of sex difference and genotypic polymorphism of ABCB1 gene encoding p-glycoprotein (involved in biliary excretion of azithromycin) on the pharmacokinetics of azithromycin has been evaluated. Azithromycin 172-184 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 32125889-1 2020 BACKGROUND: In the current study, the possible outcome of sex difference and genotypic polymorphism of ABCB1 gene encoding p-glycoprotein (involved in biliary excretion of azithromycin) on the pharmacokinetics of azithromycin has been evaluated. Azithromycin 172-184 ATP binding cassette subfamily B member 1 Homo sapiens 123-137 32125889-1 2020 BACKGROUND: In the current study, the possible outcome of sex difference and genotypic polymorphism of ABCB1 gene encoding p-glycoprotein (involved in biliary excretion of azithromycin) on the pharmacokinetics of azithromycin has been evaluated. Azithromycin 213-225 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 32125889-1 2020 BACKGROUND: In the current study, the possible outcome of sex difference and genotypic polymorphism of ABCB1 gene encoding p-glycoprotein (involved in biliary excretion of azithromycin) on the pharmacokinetics of azithromycin has been evaluated. Azithromycin 213-225 ATP binding cassette subfamily B member 1 Homo sapiens 123-137 32125889-8 2020 CONCLUSION: Gender difference and ABCB1 gene (encoding P-glycoprotein) polymorphisms have a significant impact on the pharmacokinetics of azithromycin as they contribute to inter-individual variability in therapeutic response. Azithromycin 138-150 ATP binding cassette subfamily B member 1 Homo sapiens 34-39 32125889-8 2020 CONCLUSION: Gender difference and ABCB1 gene (encoding P-glycoprotein) polymorphisms have a significant impact on the pharmacokinetics of azithromycin as they contribute to inter-individual variability in therapeutic response. Azithromycin 138-150 ATP binding cassette subfamily B member 1 Homo sapiens 55-69 32559772-9 2020 Azithromycin had the most pronounced effect on ERG1 expression in 48 and 72 h. This study indicated that these macrolides affect ERG1 expression due to their potential cardiac adverse effects. Azithromycin 0-12 potassium voltage-gated channel subfamily H member 2 Rattus norvegicus 47-51 32559772-9 2020 Azithromycin had the most pronounced effect on ERG1 expression in 48 and 72 h. This study indicated that these macrolides affect ERG1 expression due to their potential cardiac adverse effects. Azithromycin 0-12 potassium voltage-gated channel subfamily H member 2 Rattus norvegicus 129-133 31578565-7 2020 The Pb-infected mice treated with AZT/CMX exhibited decreased pulmonary concentrations of OH-proline associated with lower levels of TGF-beta1, and higher levels of IL-10 compared controls. Azithromycin 34-37 transforming growth factor, beta 1 Mus musculus 133-142 32669095-16 2020 Moreover, the mphA gene was identified in 5 of the 15 azithromycin-resistant isolates. Azithromycin 54-66 macrolide 2'-phosphotransferase I Salmonella enterica subsp. enterica serovar Typhimurium 14-18 32534189-4 2020 In vitro studies have demonstrated the capacity of azithromycin in reducing production of pro-inflammatory cytokines such as IL-8, IL-6, TNF alpha, reduce oxidative stress, and modulate T-helper functions. Azithromycin 51-63 C-X-C motif chemokine ligand 8 Homo sapiens 125-129 32534189-4 2020 In vitro studies have demonstrated the capacity of azithromycin in reducing production of pro-inflammatory cytokines such as IL-8, IL-6, TNF alpha, reduce oxidative stress, and modulate T-helper functions. Azithromycin 51-63 interleukin 6 Homo sapiens 131-135 32534189-4 2020 In vitro studies have demonstrated the capacity of azithromycin in reducing production of pro-inflammatory cytokines such as IL-8, IL-6, TNF alpha, reduce oxidative stress, and modulate T-helper functions. Azithromycin 51-63 tumor necrosis factor Homo sapiens 137-146 31578565-7 2020 The Pb-infected mice treated with AZT/CMX exhibited decreased pulmonary concentrations of OH-proline associated with lower levels of TGF-beta1, and higher levels of IL-10 compared controls. Azithromycin 34-37 interleukin 10 Mus musculus 165-170 32533263-0 2020 Intracellular ABCB1 as a Possible Mechanism to Explain the Synergistic Effect of Hydroxychloroquine-Azithromycin Combination in COVID-19 Therapy. Azithromycin 100-112 ATP binding cassette subfamily B member 1 Homo sapiens 14-19 32704543-6 2020 We also show that coadministration of lysosomotropic or lysosome-destabilizing compounds (an antibiotic azithromycin, an antidepressant siramesine, an antimalaria compound chloroquine) renders resistant tumor cells sensitive to currently used CDK4/6 inhibitors. Azithromycin 104-116 cyclin dependent kinase 4 Homo sapiens 243-249 32533263-3 2020 Azithromycin is a substrate of ABCB1 (P-glycoprotein) which is localized in endosomes and lysosomes with a polarized substrate transport from the cell cytosol into the vesicle interior. Azithromycin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 31-36 32533263-3 2020 Azithromycin is a substrate of ABCB1 (P-glycoprotein) which is localized in endosomes and lysosomes with a polarized substrate transport from the cell cytosol into the vesicle interior. Azithromycin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 32533263-7 2020 Based on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion. Azithromycin 99-111 ATP binding cassette subfamily B member 1 Homo sapiens 51-56 32511255-9 2020 RESULTS: When azithromycin (0.1, 1.0 ug/ml) was added, IL-4 levels decreased. Azithromycin 14-26 interleukin 4 Homo sapiens 55-59 32511255-12 2020 Addition of azithromycin (0.1, 1.0 ug/mL) decreased IL-4 levels and had no effect on IgE levels. Azithromycin 12-24 interleukin 4 Homo sapiens 52-56 32511255-13 2020 CONCLUSIONS: These findings indicate that azithromycin decreases IL-4 responses but has a bimodal effect on IgE responses in PBMC from atopic patients in vitro. Azithromycin 42-54 interleukin 4 Homo sapiens 65-69 32589092-5 2020 Moreover, AZM can inhibit the ability of TNF-alpha-to induce interleukin (IL)-8 production. Azithromycin 10-13 tumor necrosis factor Homo sapiens 41-50 32589092-5 2020 Moreover, AZM can inhibit the ability of TNF-alpha-to induce interleukin (IL)-8 production. Azithromycin 10-13 C-X-C motif chemokine ligand 8 Homo sapiens 61-79 32589092-6 2020 This review focuses on the effects on AZM that may be beneficial in inhibiting MUC5AC, matrix metalloprotease-9 and IL-8 production in airway epithelial cells. Azithromycin 38-41 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 79-85 32589092-6 2020 This review focuses on the effects on AZM that may be beneficial in inhibiting MUC5AC, matrix metalloprotease-9 and IL-8 production in airway epithelial cells. Azithromycin 38-41 C-X-C motif chemokine ligand 8 Homo sapiens 116-120 32307653-0 2020 CD147 as a Target for COVID-19 Treatment: Suggested Effects of Azithromycin and Stem Cell Engagement. Azithromycin 63-75 basigin (Ok blood group) Homo sapiens 0-5 32533641-4 2020 In view of established anti-proliferative properties of the macrolide antibiotic azithromycin, we examined its effects in naive mice and report a reduction in ASM thickness of 29% (p < .01). Azithromycin 81-93 H19 imprinted maternally expressed transcript Homo sapiens 159-162 32533641-8 2020 Findings provide further proof of concept that pharmacological targeting of ASM thickness will be beneficial and may be facilitated by azithromycin, revealing a new mode of action of an existing agent in respiratory medicine. Azithromycin 135-147 H19 imprinted maternally expressed transcript Homo sapiens 76-79 32307653-4 2020 Studies suggest beneficial effects of azithromycin in reducing viral load of hospitalized patients, possibly interfering with ligand/CD147 receptor interactions; however, its possible effects on SARS-CoV-2 invasion has not yet been evaluated. Azithromycin 38-50 basigin (Ok blood group) Homo sapiens 133-138 32307653-5 2020 In addition to the possible effect in invasion, azithromycin decreases the expression of some metalloproteinases (downstream to CD147), induces anti-viral responses in primary human bronchial epithelial infected with rhinovirus, decreasing viral replication and release. Azithromycin 48-60 basigin (Ok blood group) Homo sapiens 128-133 32375574-2 2021 This study demonstrated the putative inhibitory potential of lopinavir, remdesivir, oseltamir, azithromycin, ribavirin, and chloroquine towards V-ATPase, protein kinase A, SARS-CoV spike glycoprotein/ACE-2 complex and viral proteases. Azithromycin 95-107 angiotensin converting enzyme 2 Homo sapiens 200-205 32330227-11 2020 Lipid accumulation and peroxisome proliferator-activated receptor gamma (PPARgamma) expression increased in both explants and cells cultured in media containing serum or AZM. Azithromycin 170-173 peroxisome proliferator activated receptor gamma Mus musculus 23-71 32090870-4 2020 By employing an indirect electrochemical detection in the presence of 10 mM ferro/ferricyanide as redox probe, the sensor exhibited a very wide dynamic range (13.33 nM-66.67 muM), with an estimated detection limit in the subnanomolar range (0.85 nM azithromycin). Azithromycin 249-261 latexin Homo sapiens 174-177 32266043-4 2020 The sensitivity and specificity of HGF and CRP in assessing the outcome of azithromycin treatment of MP were compared using receiver operating characteristic curves. Azithromycin 75-87 hepatocyte growth factor Homo sapiens 35-38 32266043-7 2020 HGF showed higher sensitivity and specificity than CRP in assessing outcomes of azithromycin treatment of MP. Azithromycin 80-92 hepatocyte growth factor Homo sapiens 0-3 32266043-9 2020 Furthermore, HGF may be better predictive marker to assess the effectiveness of azithromycin treatment of MP than CRP. Azithromycin 80-92 hepatocyte growth factor Homo sapiens 13-16 32330227-11 2020 Lipid accumulation and peroxisome proliferator-activated receptor gamma (PPARgamma) expression increased in both explants and cells cultured in media containing serum or AZM. Azithromycin 170-173 peroxisome proliferator activated receptor gamma Mus musculus 73-82 32324238-2 2020 Objectives: To determine whether administration of azithromycin (AZM) to children with RSV-induced respiratory failure is safe and to define the effect of AZM therapy on nasal matrix metalloproteinase 9 (MMP-9) levels. Azithromycin 155-158 matrix metallopeptidase 9 Homo sapiens 176-202 31628882-7 2020 In line, a cohort study found concurrent use of clarithromycin and CYP3A4-metabolized statins to be associated with a doubled risk of hospitalization with rhabdomyolysis or other statin-related adverse events as compared with azithromycin-statin co-administration. Azithromycin 226-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 32324238-2 2020 Objectives: To determine whether administration of azithromycin (AZM) to children with RSV-induced respiratory failure is safe and to define the effect of AZM therapy on nasal matrix metalloproteinase 9 (MMP-9) levels. Azithromycin 155-158 matrix metallopeptidase 9 Homo sapiens 204-209 32324238-15 2020 Among those who required mechanical ventilation and received high-dose AZM, endotracheal active and total MMP-9 levels were lower on day 3. Azithromycin 71-74 matrix metallopeptidase 9 Homo sapiens 106-111 32324238-16 2020 Compared with baseline, active and total MMP-9 levels in endotracheal aspirates were 1.0 log lower in the high-dose AZM group (active MMP-9: 99.8% CI, -1.28 to -0.64; P < .001; total MMP-9: 99.8% CI, -1.37 to -0.57; P < .001). Azithromycin 116-119 matrix metallopeptidase 9 Homo sapiens 41-46 32324238-16 2020 Compared with baseline, active and total MMP-9 levels in endotracheal aspirates were 1.0 log lower in the high-dose AZM group (active MMP-9: 99.8% CI, -1.28 to -0.64; P < .001; total MMP-9: 99.8% CI, -1.37 to -0.57; P < .001). Azithromycin 116-119 matrix metallopeptidase 9 Homo sapiens 134-139 32324238-16 2020 Compared with baseline, active and total MMP-9 levels in endotracheal aspirates were 1.0 log lower in the high-dose AZM group (active MMP-9: 99.8% CI, -1.28 to -0.64; P < .001; total MMP-9: 99.8% CI, -1.37 to -0.57; P < .001). Azithromycin 116-119 matrix metallopeptidase 9 Homo sapiens 134-139 32324238-19 2020 While nasal MMP-9 levels were unchanged among treatment groups, endotracheal MMP-9 levels were lower among those who received high-dose AZM. Azithromycin 136-139 matrix metallopeptidase 9 Homo sapiens 77-82 31682980-3 2020 In a retrospective study of BOS patients from two large allograft centers, the effect of azithromycin exposure on the risk of relapse or SN was estimated from a Cox model with a time-dependent variable for treatment initiation. Azithromycin 89-101 cytochrome c oxidase subunit 8A Homo sapiens 161-164 32158247-11 2020 Results: Using human primary sebocytes, we found that biguanides, isotretinoin and azithromycin induced an acute dose and time-dependent increase in [14C]-acetate labeling of neutral lipids, while AICAR, an AMPK activator, inhibited this DNL response. Azithromycin 83-95 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 207-211 32519673-2 2020 Methods The immunogen AZM-BSA and coating antigen AZM-OVA were synthesized by coupling AZM to the bovine serum albumin (BSA) and ovalbumin (OVA) with the activated ester method. Azithromycin 22-25 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 129-138 32519673-5 2020 Results The titer of AZM mAb was 1:4.0x105, which belonged to IgG1 type. Azithromycin 21-24 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 62-66 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class II, DP alpha 1 Homo sapiens 89-92 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class I, A Homo sapiens 173-178 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class I, B Homo sapiens 180-185 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class II, DP alpha 1 Homo sapiens 187-195 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class II, DR alpha Homo sapiens 197-204 32218410-3 2020 The effect of azithromycin is also associated with a decrease in the expression of human HLA (human leukocyte antigen) complex molecules in the respiratory tract, including HLA-A, HLA-B, HLA-DPA1, HLA-DRA, HLA-DRB4. Azithromycin 14-26 major histocompatibility complex, class II, DR beta 4 Homo sapiens 206-214 32894857-9 2020 Five days after the last dose, serum IL-2 and IL-8 levels dropped significantly in the azithromycin group. Azithromycin 87-99 interleukin 2 Homo sapiens 37-41 31791943-3 2020 However, it has been debated whether clarithromycin and azithromycin differ in the extent to which they induce erm(41)-mediated macrolide resistance. Azithromycin 56-68 ETS variant transcription factor 5b Danio rerio 111-114 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 77-89 ETS variant transcription factor 5b Danio rerio 118-121 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 77-89 ETS variant transcription factor 5b Danio rerio 198-201 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 77-89 ETS variant transcription factor 5b Danio rerio 198-201 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 150-162 ETS variant transcription factor 5b Danio rerio 118-121 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 150-162 ETS variant transcription factor 5b Danio rerio 198-201 31791943-6 2020 Visualization of fluorescent bacilli in infected zebrafish demonstrates that azithromycin and clarithromycin activate erm(41) expression in vivo That azithromycin induces a more rapid expression of erm(41) was confirmed by measuring the beta-galactosidase activity of a reporter strain in which lacZ was placed under the control of the erm (41) promoter. Azithromycin 150-162 ETS variant transcription factor 5b Danio rerio 198-201 32449787-9 2020 Expression of YKL-40, an emerging inflammatory marker is shown to increase due to cyclical stress and by AZM treatment. Azithromycin 105-108 chitinase 3 like 1 Homo sapiens 14-20 31941499-7 2020 METHODS: Primary normal human lung and IPF-FB were exposed to TGF-beta (5 ng/ml), Azithromycin (50 muM) alone or in combination prior to gene expression analysis. Azithromycin 82-94 latexin Homo sapiens 99-102 31941499-11 2020 RESULTS: AZT significantly reduced collagen secretion in TGF-beta treated IPF-FB compared to TGF-beta treatment alone, but not in control-FB. Azithromycin 9-12 transforming growth factor beta 1 Homo sapiens 57-65 31941499-14 2020 Early apoptosis was significantly higher in TGF-beta treated IPF-FB compared to controls after AZT. Azithromycin 95-98 transforming growth factor beta 1 Homo sapiens 44-52 31941499-16 2020 The ATPase and lysosomal pH regulator ATP6V0D2 was significantly less increased after additional AZT in IPF-FB compared to controls. Azithromycin 97-100 dynein axonemal heavy chain 8 Homo sapiens 4-10 31941499-16 2020 The ATPase and lysosomal pH regulator ATP6V0D2 was significantly less increased after additional AZT in IPF-FB compared to controls. Azithromycin 97-100 ATPase H+ transporting V0 subunit d2 Homo sapiens 38-46 32894857-9 2020 Five days after the last dose, serum IL-2 and IL-8 levels dropped significantly in the azithromycin group. Azithromycin 87-99 C-X-C motif chemokine ligand 8 Homo sapiens 46-50 31512504-0 2019 Comparing the Effects of the mTOR Inhibitors Azithromycin and Rapamycin on In Vitro Expanded Regulatory T Cells. Azithromycin 45-57 mechanistic target of rapamycin kinase Homo sapiens 29-33 31512504-3 2019 Azithromycin is a bacteriostatic macrolide with mTOR inhibitory activity that has been shown to exert immunomodulatory effects on several types of immune cells. Azithromycin 0-12 mechanistic target of rapamycin kinase Homo sapiens 48-52 31512504-8 2019 Azithromycin and Rapamycin both promoted a FoxP3-positive Treg phenotype in bulk Tregs, while Rapamycin also increased FoxP3 and FoxP3+Helios positivity in naive and memory Tregs. Azithromycin 0-12 forkhead box P3 Homo sapiens 43-48 31849581-4 2019 Neuroprotection by azithromycin (150 mg/kg, i.p., upon reperfusion) was associated with a significant elevation of signal transducer and activator of transcription 3 (STAT3) phosphorylation in astrocytes and neurons of the peri-ischemic motor cortex as detected after 2 and 22 h of reperfusion. Azithromycin 19-31 signal transducer and activator of transcription 3 Rattus norvegicus 115-165 31759853-0 2019 Azithromycin suppresses Th1- and Th2-related chemokines IP-10/MDC in human monocytic cell line. Azithromycin 0-12 negative elongation factor complex member C/D Homo sapiens 24-27 31759853-0 2019 Azithromycin suppresses Th1- and Th2-related chemokines IP-10/MDC in human monocytic cell line. Azithromycin 0-12 C-X-C motif chemokine ligand 10 Homo sapiens 56-61 31759853-0 2019 Azithromycin suppresses Th1- and Th2-related chemokines IP-10/MDC in human monocytic cell line. Azithromycin 0-12 C-C motif chemokine ligand 22 Homo sapiens 62-65 31759853-3 2019 However, the effects of azithromycin on the expression of TNF-alpha, Th1- and Th2-related chemokines, and neutrophil chemoattractant are unknown. Azithromycin 24-36 tumor necrosis factor Homo sapiens 58-67 31759853-3 2019 However, the effects of azithromycin on the expression of TNF-alpha, Th1- and Th2-related chemokines, and neutrophil chemoattractant are unknown. Azithromycin 24-36 negative elongation factor complex member C/D Homo sapiens 69-72 31759853-4 2019 We investigated the in vitro effects of azithromycin on the expression of TNF-alpha, Th1-related chemokine interferon-gamma-inducible protein-10 (IP-10/CXCL10), Th2-related chemokine macrophage-derived chemokine (MDC/CCL22) and neutrophil chemoattractant growth-related oncogene-alpha (GRO-alpha/CXCL1) in THP-1 cells as a model for human monocytes. Azithromycin 40-52 tumor necrosis factor Homo sapiens 74-83 31759853-4 2019 We investigated the in vitro effects of azithromycin on the expression of TNF-alpha, Th1-related chemokine interferon-gamma-inducible protein-10 (IP-10/CXCL10), Th2-related chemokine macrophage-derived chemokine (MDC/CCL22) and neutrophil chemoattractant growth-related oncogene-alpha (GRO-alpha/CXCL1) in THP-1 cells as a model for human monocytes. Azithromycin 40-52 negative elongation factor complex member C/D Homo sapiens 85-88 31759853-4 2019 We investigated the in vitro effects of azithromycin on the expression of TNF-alpha, Th1-related chemokine interferon-gamma-inducible protein-10 (IP-10/CXCL10), Th2-related chemokine macrophage-derived chemokine (MDC/CCL22) and neutrophil chemoattractant growth-related oncogene-alpha (GRO-alpha/CXCL1) in THP-1 cells as a model for human monocytes. Azithromycin 40-52 C-X-C motif chemokine ligand 10 Homo sapiens 146-151 31654686-6 2019 NAC could be spray dried together with three different antibiotics, azithromycin (Azi), tobramycin (Tobra) and ciprofloxacin (Cipro), without the use of organic solvents to form Azi/NAC, Tobra/NAC and Cipro/NAC DPI formulations. Azithromycin 68-80 synuclein alpha Homo sapiens 0-3 31654686-6 2019 NAC could be spray dried together with three different antibiotics, azithromycin (Azi), tobramycin (Tobra) and ciprofloxacin (Cipro), without the use of organic solvents to form Azi/NAC, Tobra/NAC and Cipro/NAC DPI formulations. Azithromycin 82-85 synuclein alpha Homo sapiens 0-3 31849581-4 2019 Neuroprotection by azithromycin (150 mg/kg, i.p., upon reperfusion) was associated with a significant elevation of signal transducer and activator of transcription 3 (STAT3) phosphorylation in astrocytes and neurons of the peri-ischemic motor cortex as detected after 2 and 22 h of reperfusion. Azithromycin 19-31 signal transducer and activator of transcription 3 Rattus norvegicus 167-172 31759853-8 2019 RESULT: Azithromycin suppressed MDC and IP-10 expression in LPS-stimulated THP-1 cells. Azithromycin 8-20 C-C motif chemokine ligand 22 Homo sapiens 32-35 31759853-8 2019 RESULT: Azithromycin suppressed MDC and IP-10 expression in LPS-stimulated THP-1 cells. Azithromycin 8-20 C-X-C motif chemokine ligand 10 Homo sapiens 40-45 31759853-10 2019 Western blotting revealed that azithromycin suppressed LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK)-JNK and ERK expression, and also suppressed LPS-induced phosphorylation of nuclear factor (NF) kappaB-p65 expression. Azithromycin 31-43 mitogen-activated protein kinase 1 Homo sapiens 120-124 31759853-10 2019 Western blotting revealed that azithromycin suppressed LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK)-JNK and ERK expression, and also suppressed LPS-induced phosphorylation of nuclear factor (NF) kappaB-p65 expression. Azithromycin 31-43 mitogen-activated protein kinase 8 Homo sapiens 126-129 31759853-10 2019 Western blotting revealed that azithromycin suppressed LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK)-JNK and ERK expression, and also suppressed LPS-induced phosphorylation of nuclear factor (NF) kappaB-p65 expression. Azithromycin 31-43 mitogen-activated protein kinase 1 Homo sapiens 134-137 31759853-11 2019 CONCLUSION: Azithromycin suppressed LPS-induced MDC expression via the MAPK-JNK and the NFkappaB-p65 pathway. Azithromycin 12-24 C-C motif chemokine ligand 22 Homo sapiens 48-51 31759853-11 2019 CONCLUSION: Azithromycin suppressed LPS-induced MDC expression via the MAPK-JNK and the NFkappaB-p65 pathway. Azithromycin 12-24 mitogen-activated protein kinase 1 Homo sapiens 71-75 31759853-11 2019 CONCLUSION: Azithromycin suppressed LPS-induced MDC expression via the MAPK-JNK and the NFkappaB-p65 pathway. Azithromycin 12-24 mitogen-activated protein kinase 8 Homo sapiens 76-79 31759853-11 2019 CONCLUSION: Azithromycin suppressed LPS-induced MDC expression via the MAPK-JNK and the NFkappaB-p65 pathway. Azithromycin 12-24 RELA proto-oncogene, NF-kB subunit Homo sapiens 88-100 31759853-12 2019 Azithromycin also suppressed LPS-induced IP-10 via the MAPK-JNK/ERK and the NFkappaB-p65 pathway. Azithromycin 0-12 C-X-C motif chemokine ligand 10 Homo sapiens 41-46 31759853-12 2019 Azithromycin also suppressed LPS-induced IP-10 via the MAPK-JNK/ERK and the NFkappaB-p65 pathway. Azithromycin 0-12 mitogen-activated protein kinase 1 Homo sapiens 55-59 31759853-12 2019 Azithromycin also suppressed LPS-induced IP-10 via the MAPK-JNK/ERK and the NFkappaB-p65 pathway. Azithromycin 0-12 mitogen-activated protein kinase 8 Homo sapiens 60-63 31759853-12 2019 Azithromycin also suppressed LPS-induced IP-10 via the MAPK-JNK/ERK and the NFkappaB-p65 pathway. Azithromycin 0-12 mitogen-activated protein kinase 1 Homo sapiens 64-67 31759853-12 2019 Azithromycin also suppressed LPS-induced IP-10 via the MAPK-JNK/ERK and the NFkappaB-p65 pathway. Azithromycin 0-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 76-88 31654686-6 2019 NAC could be spray dried together with three different antibiotics, azithromycin (Azi), tobramycin (Tobra) and ciprofloxacin (Cipro), without the use of organic solvents to form Azi/NAC, Tobra/NAC and Cipro/NAC DPI formulations. Azithromycin 178-181 synuclein alpha Homo sapiens 0-3 32239863-0 2019 [Protective effects of azithromycin on adriamycin-induced nephropathy with albumin overload in mice]. Azithromycin 23-35 albumin Mus musculus 75-82 32239863-1 2019 OBJECTIVE: To study the protective effects of azithromycin on renal damage induced by doxorubicin and albumin in mice. Azithromycin 46-58 albumin Mus musculus 102-109 32239863-11 2019 CONCLUSION: Azithromycin has a protective effects on the renal damage induced by doxorubicin and albumin in mice. Azithromycin 12-24 albumin Mus musculus 97-104 31046405-0 2019 Azithromycin during Acute COPD Exacerbations Requiring Hospitalization (BACE): a Multicentre, Randomized, Double-blind, Placebo-controlled Trial. Azithromycin 0-12 beta-secretase 1 Homo sapiens 72-76 31665017-0 2019 Treatment failure and hospital readmissions in severe COPD exacerbations treated with azithromycin versus placebo - a post-hoc analysis of the BACE randomized controlled trial. Azithromycin 86-98 beta-secretase 1 Homo sapiens 143-147 31665017-1 2019 BACKGROUND: In the BACE trial, a 3-month (3 m) intervention with azithromycin, initiated at the onset of an infectious COPD exacerbation requiring hospitalization, decreased the rate of a first treatment failure (TF); the composite of treatment intensification (TI), step-up in hospital care (SH) and mortality. Azithromycin 65-77 beta-secretase 1 Homo sapiens 19-23 31665017-8 2019 CONCLUSIONS: This post-hoc analysis of the BACE trial shows that azithromycin initiated at the onset of an infectious COPD exacerbation requiring hospitalization reduces the incidence rate of TF within 3 m by preventing hospital readmissions. Azithromycin 65-77 beta-secretase 1 Homo sapiens 43-47 31527024-5 2019 In particular, we found that AZM upregulates the expression of MDA5 and RIG-I, pathogen recognition receptors (PRRs) induced by ZIKV infection, and increases the levels of phosphorylated TBK1 and IRF3. Azithromycin 29-32 TANK binding kinase 1 Homo sapiens 187-191 31527024-5 2019 In particular, we found that AZM upregulates the expression of MDA5 and RIG-I, pathogen recognition receptors (PRRs) induced by ZIKV infection, and increases the levels of phosphorylated TBK1 and IRF3. Azithromycin 29-32 interferon regulatory factor 3 Homo sapiens 196-200 31527024-6 2019 Interestingly, AZM treatment upregulates phosphorylation of TBK1, without inducing phosphorylation of IRF3 by itself. Azithromycin 15-18 TANK binding kinase 1 Homo sapiens 60-64 31894038-7 2019 In patients with ICU severe community-acquired pneumonia, the treatment of enteral nutrition support therapy combined with antibacterial drugs of azithromycin and cefuroxime sodium can effectively improve the indexes of PA, ALB and TF. Azithromycin 146-158 albumin Homo sapiens 224-227 31410140-11 2019 Compared with sequential treatment with azithromycin alone, pidotimod combined with azithromycin significantly reduced the expression levels of IL-10 and G-CSF in serum of children with mycoplasma pneumonia, improved the curative effect and reduced the occurrence of adverse reactions, which has high application value in clinic. Azithromycin 84-96 interleukin 10 Homo sapiens 144-149 31410140-11 2019 Compared with sequential treatment with azithromycin alone, pidotimod combined with azithromycin significantly reduced the expression levels of IL-10 and G-CSF in serum of children with mycoplasma pneumonia, improved the curative effect and reduced the occurrence of adverse reactions, which has high application value in clinic. Azithromycin 84-96 colony stimulating factor 3 Homo sapiens 154-159 31089818-10 2019 CONCLUSION: AZM was capable of reducing serum TNF-alpha which is one of the inflammatory cytokines implicated in the pathogenesis of NS. Azithromycin 12-15 tumor necrosis factor Homo sapiens 46-55 31894038-7 2019 In patients with ICU severe community-acquired pneumonia, the treatment of enteral nutrition support therapy combined with antibacterial drugs of azithromycin and cefuroxime sodium can effectively improve the indexes of PA, ALB and TF. Azithromycin 146-158 transferrin Homo sapiens 232-234 31263039-0 2019 Azithromycin Polarizes Macrophages to an M2 Phenotype via Inhibition of the STAT1 and NF-kappaB Signaling Pathways. Azithromycin 0-12 signal transducer and activator of transcription 1 Homo sapiens 76-81 31263039-0 2019 Azithromycin Polarizes Macrophages to an M2 Phenotype via Inhibition of the STAT1 and NF-kappaB Signaling Pathways. Azithromycin 0-12 nuclear factor kappa B subunit 1 Homo sapiens 86-95 31263039-3 2019 In this study we investigated the immunomodulatory mechanism of azithromycin through its alteration of signaling via the NF-kappaB and STAT1 pathways. Azithromycin 64-76 nuclear factor kappa B subunit 1 Homo sapiens 121-130 31263039-3 2019 In this study we investigated the immunomodulatory mechanism of azithromycin through its alteration of signaling via the NF-kappaB and STAT1 pathways. Azithromycin 64-76 signal transducer and activator of transcription 1 Homo sapiens 135-140 31263039-5 2019 The effect of azithromycin on NF-kappaB and STAT1 signaling mediators was assessed by Western blot, homogeneous time-resolved fluorescence assay, nuclear translocation assay, and immunofluorescence. Azithromycin 14-26 nuclear factor kappa B subunit 1 Homo sapiens 30-39 31263039-5 2019 The effect of azithromycin on NF-kappaB and STAT1 signaling mediators was assessed by Western blot, homogeneous time-resolved fluorescence assay, nuclear translocation assay, and immunofluorescence. Azithromycin 14-26 signal transducer and activator of transcription 1 Homo sapiens 44-49 31263039-7 2019 Azithromycin blocked NF-kappaB activation by decreasing p65 nuclear translocation, although blunting the degradation of IkappaBalpha was due, at least in part, to a decrease in IKKbeta kinase activity. Azithromycin 0-12 nuclear factor kappa B subunit 1 Homo sapiens 21-30 31263039-7 2019 Azithromycin blocked NF-kappaB activation by decreasing p65 nuclear translocation, although blunting the degradation of IkappaBalpha was due, at least in part, to a decrease in IKKbeta kinase activity. Azithromycin 0-12 RELA proto-oncogene, NF-kB subunit Homo sapiens 56-59 31263039-8 2019 A direct correlation was observed between increasing azithromycin concentrations and increased IKKbeta protein expression. Azithromycin 53-65 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 95-102 31263039-9 2019 Moreover, incubation with the IKKbeta inhibitor IKK16 decreased arginase expression and activity in azithromycin-treated cells but not in cells treated with IL-4 and IL-13. Azithromycin 100-112 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 30-37 31263039-10 2019 Importantly, azithromycin treatment also decreased STAT1 phosphorylation in a concentration-dependent manner, an effect that was reversed with IKK16 treatment. Azithromycin 13-25 signal transducer and activator of transcription 1 Homo sapiens 51-56 31263039-11 2019 We conclude that azithromycin anti-inflammatory mechanisms involve inhibition of the STAT1 and NF-kappaB signaling pathways through the drug"s effect on p65 nuclear translocation and IKKbeta. Azithromycin 17-29 signal transducer and activator of transcription 1 Homo sapiens 85-90 31263039-11 2019 We conclude that azithromycin anti-inflammatory mechanisms involve inhibition of the STAT1 and NF-kappaB signaling pathways through the drug"s effect on p65 nuclear translocation and IKKbeta. Azithromycin 17-29 nuclear factor kappa B subunit 1 Homo sapiens 95-104 31263039-11 2019 We conclude that azithromycin anti-inflammatory mechanisms involve inhibition of the STAT1 and NF-kappaB signaling pathways through the drug"s effect on p65 nuclear translocation and IKKbeta. Azithromycin 17-29 RELA proto-oncogene, NF-kB subunit Homo sapiens 153-156 31263039-11 2019 We conclude that azithromycin anti-inflammatory mechanisms involve inhibition of the STAT1 and NF-kappaB signaling pathways through the drug"s effect on p65 nuclear translocation and IKKbeta. Azithromycin 17-29 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 183-190 31382608-11 2019 In summary, azithromycin caused mitochondrial toxicity, ROS overproduction, DNA oxidative damage, upregulation of the HIF1a gene, and aerobic glycolysis in healthy mammalian cells. Azithromycin 12-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 118-123 31371681-6 2019 Azithromycin decreased the expression of IL-8 (P=0.03, one-tailed) and IL-1beta (P=0.047, one-tailed) but failed to improve the other variables evaluated. Azithromycin 0-12 C-X-C motif chemokine ligand 8 Equus caballus 41-45 31371681-6 2019 Azithromycin decreased the expression of IL-8 (P=0.03, one-tailed) and IL-1beta (P=0.047, one-tailed) but failed to improve the other variables evaluated. Azithromycin 0-12 interleukin-1 beta Equus caballus 71-79 31334131-6 2019 This compound also synergized with rifampicin and azithromycin at sub-micromolar concentrations (0.25-0.5 muM), thereby inducing susceptibility to these antibiotics at clinically relevant concentrations in clinical MDR isolates. Azithromycin 50-62 latexin Homo sapiens 106-109 30677254-8 2019 RESULTS: Azithromycin and some derivatives increased IL-10 and reduced IL-12 production of M1 macrophages. Azithromycin 9-21 interleukin 10 Homo sapiens 53-58 31798262-0 2019 Lip synechiae: A rare complication of azithromycin-associated Stevens-Johnson syndrome. Azithromycin 38-50 SMG1 nonsense mediated mRNA decay associated PI3K related kinase Homo sapiens 0-3 31063503-1 2019 AIM: Intermittent preventive treatment in pregnancy (IPTp) with azithromycin and monthly sulfadoxine-pyrimethamine increased the mean child weight, mid-upper arm and head circumference at four weeks of age in a rural low-income setting. Azithromycin 64-76 tRNA isopentenyltransferase 1 Homo sapiens 53-57 31063503-8 2019 CONCLUSION: In Malawi, IPTp with azithromycin and monthly sulfadoxine-pyrimethamine has a modest, 3-5-year positive impact on child weight, mid-upper arm circumference and head circumference, but not on weight-for-height Z-score. Azithromycin 33-45 tRNA isopentenyltransferase 1 Homo sapiens 23-27 30677254-9 2019 IL-10/IL-12 cytokine shifts closely correlated with the ability of AZM and derivatives to mitigate macrophage neurotoxicity. Azithromycin 67-70 interleukin 10 Homo sapiens 0-5 30686699-9 2019 Patients treated with azithromycin demonstrated less airway inflammation, with lower bronchoalveolar lavage (BAL) neutrophilia and BAL interleukin-8 protein levels at Day 30 (p = 0.09 and p = 0.04, respectively) and Day 90 (p = 0.002 and p = 0.08, respectively) after LTx. Azithromycin 22-34 C-X-C motif chemokine ligand 8 Homo sapiens 135-148 30925667-4 2019 The secondary structure of bovine serum albumin (BSA) was altered by the binding of drugs, like amoxicillin (Amox), cephalexin (Cefa), and azithromycin (Azit). Azithromycin 139-151 albumin Homo sapiens 34-47 30925667-4 2019 The secondary structure of bovine serum albumin (BSA) was altered by the binding of drugs, like amoxicillin (Amox), cephalexin (Cefa), and azithromycin (Azit). Azithromycin 153-157 albumin Homo sapiens 34-47 30609110-7 2019 AZM inhibited LVDCC Ca2+ permeant ion channels, M2 receptors, and TRPC3 and/or STIM/Orai, which decreased cytosolic Ca2+ concentrations and led to muscle relaxation. Azithromycin 0-3 transient receptor potential cation channel subfamily C member 3 Homo sapiens 66-71 30445620-8 2019 Their second and third patients received Azithromycin targeting IL-17A and showed clinical responses. Azithromycin 41-53 interleukin 17A Homo sapiens 64-70 30530046-0 2019 Azithromycin treats diffuse panbronchiolitis by targeting T cells via inhibition of mTOR pathway. Azithromycin 0-12 mechanistic target of rapamycin kinase Homo sapiens 84-88 30530046-5 2019 AZM and EM significantly inhibited IL-17A and CXCL-2 production in patients" PBLs (all P < 0.05). Azithromycin 0-3 interleukin 17A Homo sapiens 35-41 30530046-5 2019 AZM and EM significantly inhibited IL-17A and CXCL-2 production in patients" PBLs (all P < 0.05). Azithromycin 0-3 C-X-C motif chemokine ligand 2 Homo sapiens 46-52 30530046-7 2019 AZM can enhance autophagosome formation of T cells by suppressing S6RP phosphorylation, which is a downstream target of mTOR pathway (all P < 0.05). Azithromycin 0-3 mechanistic target of rapamycin kinase Homo sapiens 120-124 30530046-8 2019 AZM and EM significantly decreased secreted IL-17A levels (P < 0.05) in the primary CD4 + T cells of patients with DPB. Azithromycin 0-3 interleukin 17A Homo sapiens 44-50 30530046-10 2019 The mechanism of therapeutic effects of AZM on DPB may be associated with a specific inhibition of mTOR pathway in the T lymphocytes. Azithromycin 40-43 mechanistic target of rapamycin kinase Homo sapiens 99-103 30608101-5 2019 The acid-labile release of d-tyrosine disintegrated the biofilm matrix, and the lipase-triggered release of azithromycin eradicated the bacteria in the biofilms. Azithromycin 108-120 lipase G, endothelial type Rattus norvegicus 80-86 30515223-9 2018 AZM enhanced the osteogenic differentiation of PDLSCs that were stimulated with TNF-alpha. Azithromycin 0-3 tumor necrosis factor Homo sapiens 80-89 30460724-0 2019 Effect of antenatal azithromycin for Ureaplasma spp. Azithromycin 20-32 histocompatibility minor 13 Homo sapiens 48-51 30391117-1 2018 Although azithromycin can suppress cardiac INa, IKr, IKs, ICa,L and IK1, its onset mechanisms for cardiovascular death have not been fully investigated. Azithromycin 9-21 IKAROS family zinc finger 1 Homo sapiens 68-71 30515223-0 2018 Azithromycin Promotes the Osteogenic Differentiation of Human Periodontal Ligament Stem Cells after Stimulation with TNF-alpha. Azithromycin 0-12 tumor necrosis factor Homo sapiens 117-126 30011231-4 2019 The potency of the broad-spectrum antibiotics, tobramycin, levofloxacin, and azithromycin on the highly expressed T2Rs in airways, T2R4, T2R14, and T2R20 was pursued. Azithromycin 77-89 taste 2 receptor member 14 Homo sapiens 137-142 30011231-4 2019 The potency of the broad-spectrum antibiotics, tobramycin, levofloxacin, and azithromycin on the highly expressed T2Rs in airways, T2R4, T2R14, and T2R20 was pursued. Azithromycin 77-89 taste 2 receptor member 20 Homo sapiens 148-153 30264382-0 2018 Effect of Azithromycin on Venetoclax Pharmacokinetics in Healthy Volunteers: Implications for Dosing Venetoclax with P-gp Inhibitors. Azithromycin 10-22 ATP binding cassette subfamily B member 1 Homo sapiens 117-121 30515223-10 2018 Western blot analysis showed that beta-catenin, phosphorated p65, and phosphorylated IkappaB-alpha protein expression decreased in PDLSCs treated with AZM. Azithromycin 151-154 catenin beta 1 Homo sapiens 34-46 30515223-1 2018 Background and Objective: This study investigated the effects and underlying mechanisms of azithromycin (AZM) treatment on the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) after their stimulation with TNF-alpha in vitro. Azithromycin 91-103 tumor necrosis factor Homo sapiens 233-242 30515223-1 2018 Background and Objective: This study investigated the effects and underlying mechanisms of azithromycin (AZM) treatment on the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) after their stimulation with TNF-alpha in vitro. Azithromycin 105-108 tumor necrosis factor Homo sapiens 233-242 30515223-10 2018 Western blot analysis showed that beta-catenin, phosphorated p65, and phosphorylated IkappaB-alpha protein expression decreased in PDLSCs treated with AZM. Azithromycin 151-154 RELA proto-oncogene, NF-kB subunit Homo sapiens 61-64 30515223-10 2018 Western blot analysis showed that beta-catenin, phosphorated p65, and phosphorylated IkappaB-alpha protein expression decreased in PDLSCs treated with AZM. Azithromycin 151-154 NFKB inhibitor alpha Homo sapiens 85-98 30515223-11 2018 In addition, pretreatment of PDLSCs with AZM (10 mug/ml, 20 mug/ml) prevented TNF-alpha-induced apoptosis by decreasing caspase-8 and caspase-3 expression. Azithromycin 41-44 tumor necrosis factor Homo sapiens 78-87 30515223-11 2018 In addition, pretreatment of PDLSCs with AZM (10 mug/ml, 20 mug/ml) prevented TNF-alpha-induced apoptosis by decreasing caspase-8 and caspase-3 expression. Azithromycin 41-44 caspase 8 Homo sapiens 120-129 30515223-11 2018 In addition, pretreatment of PDLSCs with AZM (10 mug/ml, 20 mug/ml) prevented TNF-alpha-induced apoptosis by decreasing caspase-8 and caspase-3 expression. Azithromycin 41-44 caspase 3 Homo sapiens 134-143 30515223-12 2018 Conclusions: Our results showed that AZM promotes PDLSCs osteogenic differentiation in an inflammatory microenvironment by inhibiting the WNT and NF-kappaB signaling pathways and by suppressing TNF-alpha-induced apoptosis. Azithromycin 37-40 tumor necrosis factor Homo sapiens 194-203 30348950-0 2018 Azithromycin promotes alternatively activated macrophage phenotype in systematic lupus erythematosus via PI3K/Akt signaling pathway. Azithromycin 0-12 AKT serine/threonine kinase 1 Homo sapiens 110-113 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 AKT serine/threonine kinase 1 Homo sapiens 79-82 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 AKT serine/threonine kinase 1 Homo sapiens 136-139 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 interleukin 1 alpha Homo sapiens 198-206 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 interleukin 6 Homo sapiens 208-212 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 tumor necrosis factor Homo sapiens 218-227 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 mannose receptor C-type 1 Homo sapiens 297-302 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 arginase 1 Homo sapiens 304-309 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 resistin like beta Homo sapiens 311-317 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 0-12 interleukin 10 Homo sapiens 323-328 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 238-250 AKT serine/threonine kinase 1 Homo sapiens 136-139 30348950-9 2018 Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1beta, IL-6, and TNF-alpha caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Azithromycin 336-348 AKT serine/threonine kinase 1 Homo sapiens 136-139 30334401-0 2018 Azithromycin influences airway remodeling in asthma via the PI3K/Akt/MTOR/HIF-1alpha/VEGF pathway. Azithromycin 0-12 AKT serine/threonine kinase 1 Homo sapiens 65-68 30334401-0 2018 Azithromycin influences airway remodeling in asthma via the PI3K/Akt/MTOR/HIF-1alpha/VEGF pathway. Azithromycin 0-12 mechanistic target of rapamycin kinase Homo sapiens 69-73 30334401-0 2018 Azithromycin influences airway remodeling in asthma via the PI3K/Akt/MTOR/HIF-1alpha/VEGF pathway. Azithromycin 0-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 74-84 30334401-0 2018 Azithromycin influences airway remodeling in asthma via the PI3K/Akt/MTOR/HIF-1alpha/VEGF pathway. Azithromycin 0-12 vascular endothelial growth factor A Homo sapiens 85-89 30334401-8 2018 In this study, we investigated the protective effect of azithromycin on airway remodeling through the phosphoinositol-3 kinase/Akt/mechanistic target of rapamycin kinase/hypoxia-inducible factor 1alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) pathway. Azithromycin 56-68 AKT serine/threonine kinase 1 Homo sapiens 127-130 30334401-8 2018 In this study, we investigated the protective effect of azithromycin on airway remodeling through the phosphoinositol-3 kinase/Akt/mechanistic target of rapamycin kinase/hypoxia-inducible factor 1alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) pathway. Azithromycin 56-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 203-213 30334401-8 2018 In this study, we investigated the protective effect of azithromycin on airway remodeling through the phosphoinositol-3 kinase/Akt/mechanistic target of rapamycin kinase/hypoxia-inducible factor 1alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) pathway. Azithromycin 56-68 vascular endothelial growth factor A Homo sapiens 215-249 30334401-8 2018 In this study, we investigated the protective effect of azithromycin on airway remodeling through the phosphoinositol-3 kinase/Akt/mechanistic target of rapamycin kinase/hypoxia-inducible factor 1alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) pathway. Azithromycin 56-68 vascular endothelial growth factor A Homo sapiens 251-255 30334401-10 2018 Gene expression analysis confirmed that HIF-1alpha and VEGF were significantly down-regulated following a long course of azithromycin administration. Azithromycin 121-133 hypoxia inducible factor 1 subunit alpha Homo sapiens 40-50 30334401-10 2018 Gene expression analysis confirmed that HIF-1alpha and VEGF were significantly down-regulated following a long course of azithromycin administration. Azithromycin 121-133 vascular endothelial growth factor A Homo sapiens 55-59 29689527-9 2018 The results showed that zeolites with FAU structure can be used as effective adsorbents for the removal of antibiotics with different physicochemical properties, including molecules with large volumes, such as azithromycin. Azithromycin 210-222 FAU ubiquitin like and ribosomal protein S30 fusion Homo sapiens 38-41 29941652-9 2018 Covariate analysis verified that body weight and alanine aminotransferase (ALT) had significant effects on azithromycin pharmacokinetics, yielding a 24% decrease of clearance in patients with ALT of >40. Azithromycin 107-119 glutamic--pyruvic transaminase Homo sapiens 49-73 29970185-13 2018 Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL. Azithromycin 0-12 TNF receptor superfamily member 10a Homo sapiens 42-45 29970185-14 2018 Knockdown of DR4 and DR5 with siRNAs increased cell survival rate and decreased the expression of cleaved-PARP induced by the combination of azithromycin and TRAIL. Azithromycin 141-153 TNF receptor superfamily member 10b Homo sapiens 21-24 29970185-14 2018 Knockdown of DR4 and DR5 with siRNAs increased cell survival rate and decreased the expression of cleaved-PARP induced by the combination of azithromycin and TRAIL. Azithromycin 141-153 poly(ADP-ribose) polymerase 1 Homo sapiens 106-110 29970185-16 2018 CONCLUSION: The synergistic antitumor effect of azithromycin and TRAIL mainly relies on the up-regulations of DR4 and DR5, which in turn result from LC-3B-involved autophagy inhibition. Azithromycin 48-60 TNF receptor superfamily member 10a Homo sapiens 110-113 29970185-16 2018 CONCLUSION: The synergistic antitumor effect of azithromycin and TRAIL mainly relies on the up-regulations of DR4 and DR5, which in turn result from LC-3B-involved autophagy inhibition. Azithromycin 48-60 TNF receptor superfamily member 10b Homo sapiens 118-121 30001416-9 2018 AZM-treated mice showed a significant decrease in pro-inflammatory (CD45+/Ly6G-/F4-80+/CD86+) and increase in anti-inflammatory (CD45+/Ly6G-/F4-80+/CD206+) macrophages, decreasing the pro-inflammatory/anti-inflammatory macrophage ratio in the heart and peripheral blood as assessed by flow cytometry and immunohistochemistry. Azithromycin 0-3 lymphocyte antigen 6 complex, locus G Mus musculus 74-78 29970185-16 2018 CONCLUSION: The synergistic antitumor effect of azithromycin and TRAIL mainly relies on the up-regulations of DR4 and DR5, which in turn result from LC-3B-involved autophagy inhibition. Azithromycin 48-60 microtubule associated protein 1 light chain 3 beta Homo sapiens 149-154 30001416-9 2018 AZM-treated mice showed a significant decrease in pro-inflammatory (CD45+/Ly6G-/F4-80+/CD86+) and increase in anti-inflammatory (CD45+/Ly6G-/F4-80+/CD206+) macrophages, decreasing the pro-inflammatory/anti-inflammatory macrophage ratio in the heart and peripheral blood as assessed by flow cytometry and immunohistochemistry. Azithromycin 0-3 lymphocyte antigen 6 complex, locus G Mus musculus 135-139 29463692-7 2018 Azithromycin and erythromycin showed the greatest effect in subjects with COPD, with evidence suggesting improvement in exacerbation-related outcomes and health status, as measured by the St George Respiratory Questionnaire. Azithromycin 0-12 COPD Homo sapiens 74-78 29624919-9 2018 In comparison, NL of PsA-chron patients revealed generally lower IL-8 and IL-1beta concentrations as in PsA-free patients, most likely due to a consequent antibiotic and anti-inflammatory therapy (eg, with azithromycin). Azithromycin 206-218 interleukin 1 beta Homo sapiens 74-82 29914941-8 2018 Combination therapy with an AZM-SPR741 HSR showed promising in vivo activity against MDR Enterobacteriaceae isolates with AZM MICs of <=16 mg/liter, including those producing a variety of beta-lactamases. Azithromycin 28-31 sepiapterin reductase Mus musculus 32-35 29879240-0 2018 Clinical Inquiries: Does prophylactic azithromycin reduce the number of COPD exacerbations or hospitalizations? Azithromycin 38-50 COPD Homo sapiens 72-76 29879240-4 2018 Azithromycin benefits patients who are >65 years, patients with Global Initiative for Obstructive Lung Disease (GOLD) stage II or III COPD, former smokers, and patients using long-term oxygen; it doesn"t benefit patients <=65 years, patients with GOLD stage IV COPD, current smokers, or patients not using oxygen (strength of recommendation [SOR]: B, randomized controlled trials [RCTs]). Azithromycin 0-12 COPD Homo sapiens 137-141 29879240-4 2018 Azithromycin benefits patients who are >65 years, patients with Global Initiative for Obstructive Lung Disease (GOLD) stage II or III COPD, former smokers, and patients using long-term oxygen; it doesn"t benefit patients <=65 years, patients with GOLD stage IV COPD, current smokers, or patients not using oxygen (strength of recommendation [SOR]: B, randomized controlled trials [RCTs]). Azithromycin 0-12 COPD Homo sapiens 267-271 29970185-0 2018 Azithromycin enhances anticancer activity of TRAIL by inhibiting autophagy and up-regulating the protein levels of DR4/5 in colon cancer cells in vitro and in vivo. Azithromycin 0-12 TNF superfamily member 10 Homo sapiens 45-50 29970185-0 2018 Azithromycin enhances anticancer activity of TRAIL by inhibiting autophagy and up-regulating the protein levels of DR4/5 in colon cancer cells in vitro and in vivo. Azithromycin 0-12 TNF receptor superfamily member 10a Homo sapiens 115-120 29970185-13 2018 Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL. Azithromycin 0-12 TNF receptor superfamily member 10b Homo sapiens 47-50 29970185-13 2018 Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL. Azithromycin 0-12 nucleoporin 62 Homo sapiens 52-55 29970185-13 2018 Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL. Azithromycin 0-12 microtubule associated protein 1 light chain 3 beta Homo sapiens 60-65 29970185-13 2018 Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL. Azithromycin 0-12 TNF superfamily member 10 Homo sapiens 117-122 29970185-14 2018 Knockdown of DR4 and DR5 with siRNAs increased cell survival rate and decreased the expression of cleaved-PARP induced by the combination of azithromycin and TRAIL. Azithromycin 141-153 TNF receptor superfamily member 10a Homo sapiens 13-16 29794203-8 2018 Azithromycin is the principal macrolide used chronically for obstructive lung diseases, especially COPD. Azithromycin 0-12 COPD Homo sapiens 99-103 29880387-0 2018 Azithromycin Fails to Prevent Accelerated Airway Obliteration in T-bet-/- Mouse Lung Allograft Recipients. Azithromycin 0-12 T-box 21 Mus musculus 65-70 29880387-9 2018 RESULTS: We show that while azithromycin significantly decreases lung allograft neutrophilia and CXCL1 levels and attenuates allospecific CD8+ IL-17 responses early post-transplantation, OAD persists in T-bet-deficient mice. Azithromycin 28-40 chemokine (C-X-C motif) ligand 1 Mus musculus 97-102 29880387-9 2018 RESULTS: We show that while azithromycin significantly decreases lung allograft neutrophilia and CXCL1 levels and attenuates allospecific CD8+ IL-17 responses early post-transplantation, OAD persists in T-bet-deficient mice. Azithromycin 28-40 interleukin 17A Mus musculus 143-148 29567590-2 2018 In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice. Azithromycin 36-48 transforming growth factor, beta 1 Mus musculus 184-217 29567590-2 2018 In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice. Azithromycin 36-48 transforming growth factor, beta 1 Mus musculus 219-228 29567590-2 2018 In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice. Azithromycin 36-48 receptor for activated C kinase 1 Mus musculus 230-262 29567590-2 2018 In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice. Azithromycin 36-48 receptor for activated C kinase 1 Mus musculus 264-269 29567590-2 2018 In this study, we hypothesized that azithromycin (35 mg/kg orally) alleviated airway remodeling through suppression of epithelial-to-mesenchymal transition (EMT) via downregulation of transforming growth factor-beta 1 (TGF-beta1)/receptor for activated C-kinase1 (RACK1)/snail in mice. Azithromycin 36-48 snail family zinc finger 1 Mus musculus 271-276 29567590-6 2018 Our data showed that azithromycin significantly reduced inflammation score, peribronchial smooth muscle layer thickness, goblet cell metaplasia, and deposition of collage fibers (P < 0.05), and effectively suppressed airway EMT (upregulated E-cadherin level, and downregulated N-cadherin and alpha-SMA levels) compared with the OVA group (P < 0.05). Azithromycin 21-33 cadherin 1 Mus musculus 244-254 29567590-6 2018 Our data showed that azithromycin significantly reduced inflammation score, peribronchial smooth muscle layer thickness, goblet cell metaplasia, and deposition of collage fibers (P < 0.05), and effectively suppressed airway EMT (upregulated E-cadherin level, and downregulated N-cadherin and alpha-SMA levels) compared with the OVA group (P < 0.05). Azithromycin 21-33 cadherin 2 Mus musculus 280-290 29567590-6 2018 Our data showed that azithromycin significantly reduced inflammation score, peribronchial smooth muscle layer thickness, goblet cell metaplasia, and deposition of collage fibers (P < 0.05), and effectively suppressed airway EMT (upregulated E-cadherin level, and downregulated N-cadherin and alpha-SMA levels) compared with the OVA group (P < 0.05). Azithromycin 21-33 actin alpha 2, smooth muscle, aorta Mus musculus 295-304 29567590-7 2018 Moreover, the increasing mRNA and protein expressions of TGF-beta1 and RACK1 and mRNA level of Snail in lung tissue were all significantly decreased in azithromycin-treated mice (P < 0.05). Azithromycin 152-164 transforming growth factor, beta 1 Mus musculus 57-66 29567590-7 2018 Moreover, the increasing mRNA and protein expressions of TGF-beta1 and RACK1 and mRNA level of Snail in lung tissue were all significantly decreased in azithromycin-treated mice (P < 0.05). Azithromycin 152-164 receptor for activated C kinase 1 Mus musculus 71-76 29567590-7 2018 Moreover, the increasing mRNA and protein expressions of TGF-beta1 and RACK1 and mRNA level of Snail in lung tissue were all significantly decreased in azithromycin-treated mice (P < 0.05). Azithromycin 152-164 snail family zinc finger 1 Mus musculus 95-100 29567590-8 2018 Taken together, our results suggest that azithromycin has the greatest effects on reducing airway remodeling by inhibiting TGF-beta1/RACK1/Snail signal and improving the EMT in airway epithelium. Azithromycin 41-53 transforming growth factor, beta 1 Mus musculus 123-132 29567590-8 2018 Taken together, our results suggest that azithromycin has the greatest effects on reducing airway remodeling by inhibiting TGF-beta1/RACK1/Snail signal and improving the EMT in airway epithelium. Azithromycin 41-53 receptor for activated C kinase 1 Mus musculus 133-138 29567590-8 2018 Taken together, our results suggest that azithromycin has the greatest effects on reducing airway remodeling by inhibiting TGF-beta1/RACK1/Snail signal and improving the EMT in airway epithelium. Azithromycin 41-53 snail family zinc finger 1 Mus musculus 139-144 29373697-5 2018 The observed resistance was attributable to one of two different azithromycin resistance mechanisms; the 23S rRNA C2611T mutation was identified in 24% of isolates, whereas the majority of resistance (76%) was associated with a meningococcal-type mtrR variant. Azithromycin 65-77 5-methyltetrahydrofolate-homocysteine methyltransferase reductase Homo sapiens 247-251 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 tumor necrosis factor Homo sapiens 27-30 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 interleukin 1 beta Homo sapiens 32-40 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 interleukin 6 Homo sapiens 42-46 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 interleukin 10 Homo sapiens 51-56 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 interleukin 1 beta Homo sapiens 74-82 29715306-10 2018 AZI inhibited R848-induced TNF, IL-1beta, IL-6 and IL-10, and LPS-induced IL-1beta and IL-10. Azithromycin 0-3 interleukin 10 Homo sapiens 87-92