PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8418915-6 1993 Treatment of murine decidual explants with LPS, IL-1 beta, and TNF resulted in significant increases in the production of prostaglandin E2 (PGE2) and IL-6. Dinoprostone 122-138 toll-like receptor 4 Mus musculus 43-46 8418915-6 1993 Treatment of murine decidual explants with LPS, IL-1 beta, and TNF resulted in significant increases in the production of prostaglandin E2 (PGE2) and IL-6. Dinoprostone 140-144 toll-like receptor 4 Mus musculus 43-46 8418915-7 1993 Thus the regulation of PGE2 and IL-6 production from murine decidua by LPS and inflammatory cytokines is similar to findings previously reported for human decidua. Dinoprostone 23-27 toll-like receptor 4 Mus musculus 71-74 1382857-6 1992 Altogether these data show that when splenocytes are cultured for more than 72 h in the presence of IL-2 and LPS their cytotoxic activity decreases, and it is likely that this diminution is linked to the endogenous production of prostaglandin E2 and INF alpha/beta. Dinoprostone 229-245 toll-like receptor 4 Mus musculus 109-112 1379986-8 1992 Prostaglandin E2 synthesis by macrophages was also blocked by LPS. Dinoprostone 0-16 toll-like receptor 4 Mus musculus 62-65 1314222-8 1992 Furthermore, the anti-L. pneumophila activity of macrophages induced by LPS could also be reversed in vitro by treatment with prostaglandin E2, colchicine, isoproterenol, theophylline, or hydrocortisone, all of which are known to increase the intracellular levels of cyclic AMP in various tissues. Dinoprostone 126-142 toll-like receptor 4 Mus musculus 72-75 2172382-1 1990 The influence of PGE2 and the consequent rise in intracellular cAMP on LPS-induced IL-1 alpha and IL-1 beta mRNA levels has been examined in murine peritoneal macrophages. Dinoprostone 17-21 toll-like receptor 4 Mus musculus 71-74 1918061-4 1991 Complete, apparently competitive, inhibition of LPS activity is possible at a 10-100-fold excess of antagonist, as judged by measuring the release of cytokines and prostaglandin E2. Dinoprostone 164-180 toll-like receptor 4 Mus musculus 48-51 2172382-5 1990 PGE2 and dBcAMP not only potentiated LPS-induced IL-1 beta mRNA levels but were also able to stimulate modest accumulation of IL-1 beta mRNA in the absence of LPS. Dinoprostone 0-4 toll-like receptor 4 Mus musculus 37-40 2120289-2 1990 Mouse peritoneal macrophages from LPS-treated animals showed a two to three fold increase in COX activity determined by the production of PGE2 and PGI2 after stimulation of the cells with exogenous arachidonate. Dinoprostone 138-142 toll-like receptor 4 Mus musculus 34-37 6300968-1 1982 Mouse resident peritoneal macrophages stimulated in vitro by purified bacterial lipopolysaccharide (LPS) produced both prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2), the latter detected as its stable metabolite, 6-keto PGF1 alpha. Dinoprostone 119-135 toll-like receptor 4 Mus musculus 100-103 2172382-6 1990 Although measurement of IL-1 activity by bioassay suggested that dBcAMP and PGE2 could suppress LPS-induced IL-1 expression, levels of IL-1 protein, determined by radioreceptor assay, were markedly elevated. Dinoprostone 76-80 toll-like receptor 4 Mus musculus 96-99 34725110-6 2021 The Acsl4-deficient rpMACs stimulated with opZym also demonstrated an acute reduction in mRNA expression of the inflammatory cytokines, Il6, Ccl2, Nos2, and Ccl5 When Acsl4-deficient rpMACs were incubated in vitro with the TLR4 agonist, LPS, the levels of leukotriene B4 and PGE2 were also significantly decreased. Dinoprostone 275-279 toll-like receptor 4 Mus musculus 223-227 2549293-8 1989 LPS caused a dose-dependent increase of PGE2 synthesis by mesangial cells. Dinoprostone 40-44 toll-like receptor 4 Mus musculus 0-3 2547721-1 1989 The regulation of lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF) production by prostaglandin E2 (PGE2), forskolin, and dibutyryl cyclic AMP (cAMP) was examined at the cellular and molecular levels. Dinoprostone 99-115 toll-like receptor 4 Mus musculus 38-41 2547721-1 1989 The regulation of lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF) production by prostaglandin E2 (PGE2), forskolin, and dibutyryl cyclic AMP (cAMP) was examined at the cellular and molecular levels. Dinoprostone 117-121 toll-like receptor 4 Mus musculus 38-41 2547721-3 1989 The concomitant addition of PGE2, dibutyryl cAMP, or forskolin to LPS-challenged M phi s resulted in 50% inhibition of TNF production at 10(-7), 3 X 10(-6), and 3 X 10(-5) M, respectively. Dinoprostone 28-32 toll-like receptor 4 Mus musculus 66-69 2547721-4 1989 Interestingly, delaying the addition of PGE2 or dibutyryl cAMP by 1.5 h post-LPS stimulation was also effective in suppressing the production of TNF bioactivity, but only dibutyryl cAMP was effective when its addition was delayed by 3 h. Northern (RNA) blot analysis of mRNA isolated from LPS-challenged M phi s treated with PGE2 or dibutyryl cAMP corroborated the bioactivity data. Dinoprostone 40-44 toll-like receptor 4 Mus musculus 77-80 2547721-4 1989 Interestingly, delaying the addition of PGE2 or dibutyryl cAMP by 1.5 h post-LPS stimulation was also effective in suppressing the production of TNF bioactivity, but only dibutyryl cAMP was effective when its addition was delayed by 3 h. Northern (RNA) blot analysis of mRNA isolated from LPS-challenged M phi s treated with PGE2 or dibutyryl cAMP corroborated the bioactivity data. Dinoprostone 40-44 toll-like receptor 4 Mus musculus 289-292 2547721-5 1989 The delayed addition of PGE2 or dibutyryl cAMP by 1.5 h post-LPS stimulation resulted in a suppression of TNF mRNA accumulation by 50 to 70%. Dinoprostone 24-28 toll-like receptor 4 Mus musculus 61-64 2424900-6 1986 Suppression of LPS-induced IL 1 production by PGE2 was prevented by leukocyte alpha-interferon. Dinoprostone 46-50 toll-like receptor 4 Mus musculus 15-18 6350291-8 1983 Although LPS stimulates prostaglandin E2 synthesis, prostaglandin E2 itself did not suppress apo-E synthesis. Dinoprostone 24-40 toll-like receptor 4 Mus musculus 9-12 6300968-1 1982 Mouse resident peritoneal macrophages stimulated in vitro by purified bacterial lipopolysaccharide (LPS) produced both prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2), the latter detected as its stable metabolite, 6-keto PGF1 alpha. Dinoprostone 137-141 toll-like receptor 4 Mus musculus 100-103 6300968-2 1982 Maximum production, induced in each case by 1 ng/ml purified LPS, was in the range of 10(-7)M for PGI2 and 3 x 10(-8)M for PGE2. Dinoprostone 123-127 toll-like receptor 4 Mus musculus 61-64 34034779-0 2021 Involvement of TLR4 signaling regulated-COX2/PGE2 axis in liver fibrosis induced by Schistosoma japonicum infection. Dinoprostone 45-49 toll-like receptor 4 Mus musculus 15-19 6267131-7 1981 This inhibitory effect of PGE2 on the LPS-induced activation of macrophages could be reproduced by cyclic-adenosine-monophosphate (cAMP) agonists, such as isoproterenol and cholera toxin as well as by the cAMP analog dibutyryl-cAMP, suggesting a cAMP-mediated mechanism for the inhibitory effect of PGE2 on macrophage activation by LPS. Dinoprostone 299-303 toll-like receptor 4 Mus musculus 38-41 7451984-8 1981 The latter effect could be reversed by adding PGE2 to the cultures at a concentration of 10(-8) M. Lastly, PGE inhibited cytolytic activity mediated by indomethacin-treated macrophages only when activator was present: pulsing with PGE before the addition of LPS had a negligible inhibitory effect. Dinoprostone 46-50 toll-like receptor 4 Mus musculus 258-261 6267131-0 1981 Regulation by PGE2 of the production of oxygen intermediates by LPS-activated macrophages. Dinoprostone 14-18 toll-like receptor 4 Mus musculus 64-67 6267131-1 1981 The regulation by prostaglandin E2 (PGE2) of production of oxygen radicals by bacterial lipopolysaccharide-(LPS) activated macrophages was studied in vitro. Dinoprostone 18-34 toll-like receptor 4 Mus musculus 108-111 6267131-1 1981 The regulation by prostaglandin E2 (PGE2) of production of oxygen radicals by bacterial lipopolysaccharide-(LPS) activated macrophages was studied in vitro. Dinoprostone 36-40 toll-like receptor 4 Mus musculus 108-111 6267131-5 1981 The PMA-triggered production of oxygen radicals by the LPS-activated macrophages was inhibited when PGE2 (10(-5) to 10(-9) M) was present during the incubation with LPS. Dinoprostone 100-104 toll-like receptor 4 Mus musculus 55-58 6267131-5 1981 The PMA-triggered production of oxygen radicals by the LPS-activated macrophages was inhibited when PGE2 (10(-5) to 10(-9) M) was present during the incubation with LPS. Dinoprostone 100-104 toll-like receptor 4 Mus musculus 165-168 6267131-6 1981 Inhibition by PGE2 occurred during the early stages of macrophage activation, since the addition of PGE2 24 hr after LPS no longer inhibited the production of oxygen radicals by the macrophages. Dinoprostone 14-18 toll-like receptor 4 Mus musculus 117-120 6267131-7 1981 This inhibitory effect of PGE2 on the LPS-induced activation of macrophages could be reproduced by cyclic-adenosine-monophosphate (cAMP) agonists, such as isoproterenol and cholera toxin as well as by the cAMP analog dibutyryl-cAMP, suggesting a cAMP-mediated mechanism for the inhibitory effect of PGE2 on macrophage activation by LPS. Dinoprostone 26-30 toll-like receptor 4 Mus musculus 38-41 6267131-7 1981 This inhibitory effect of PGE2 on the LPS-induced activation of macrophages could be reproduced by cyclic-adenosine-monophosphate (cAMP) agonists, such as isoproterenol and cholera toxin as well as by the cAMP analog dibutyryl-cAMP, suggesting a cAMP-mediated mechanism for the inhibitory effect of PGE2 on macrophage activation by LPS. Dinoprostone 26-30 toll-like receptor 4 Mus musculus 332-335 34034779-11 2021 TLR4 pathway activation stimulated the COX2/PGE2 axis in Sj-infected mice and in lipopolysaccharide (LPS)-exposed cultured HSCs. Dinoprostone 44-48 toll-like receptor 4 Mus musculus 0-4 34034779-15 2021 TLR4 signaling may at least partially control the COX2/PGE2 axis in Sj-infected mice liver and in vitro cultured HSCs. Dinoprostone 55-59 toll-like receptor 4 Mus musculus 0-4 33283918-5 2021 There was significant upregulation of inflammatory markers like COX-2, PGE2 , S100A8, and S100A9 in the skin of TLR4-proficient mice than the skin of TLR4-deficient mice. Dinoprostone 71-75 toll-like receptor 4 Mus musculus 112-116 33552081-5 2020 Hyaluronic acid binding to TLR4 in pericryptal macrophages results in cyclooxygenase2- dependent PGE2 production, which transactivates EGFR in LGR5+ crypt epithelial stem cells leading to increased proliferation. Dinoprostone 97-101 toll-like receptor 4 Mus musculus 27-31 31999624-5 2020 In pregnant mice uterus, EE reduces the expression of TLR4 and CD14 (the LPS receptor and its coactivator protein), preventing the LPS-induced increase in PGE2 and PGF2alpha release and nitric oxide synthase (NOS) activity. Dinoprostone 155-159 toll-like receptor 4 Mus musculus 54-58 32538139-10 2020 We conclude that, in postnatal mice, ~30% of intestinal growth as manifested by crypt fission and Lgr5+ stem cell proliferation is driven by a novel pathway: Extracellular HA binds TLR4 on pericryptal macrophages, inducing the production of PGE2 through COX2. Dinoprostone 241-245 toll-like receptor 4 Mus musculus 181-185 32538139-12 2020 In this pathway, endogenous extracellular hyaluronic acid binds to Toll-like receptor 4 on pericryptal macrophages releasing PGE2 which binds to epidermal growth factor receptor on Lgr5+ stem cells resulting in proliferation. Dinoprostone 125-129 toll-like receptor 4 Mus musculus 67-87 31879211-0 2020 Inhibitory effects of triarylpyrazole derivatives on LPS-induced nitric oxide and PGE2 productions in murine RAW 264.7 macrophages. Dinoprostone 82-86 toll-like receptor 4 Mus musculus 53-56 31141808-8 2020 Thus, macrophage PGE2 secretion after S. aureus infection depends on bacterial lipoprotein maturation and macrophage receptors TLR2, TLR4, and NLRP3. Dinoprostone 17-21 toll-like receptor 4 Mus musculus 133-137 30724376-5 2019 The results showed that LPS significantly activated the BV2 cells via toll-like receptor 4 to induce elevated productions of ROS, NO, PGE2, IL-6, and IL-1beta. Dinoprostone 134-138 toll-like receptor 4 Mus musculus 70-90 31772309-4 2019 Using mice lacking TLR2 and TLR4 in combination, here we show that social defeat stress (SDS) induced the PGE2 synthesis in subcortical, but not cortical, tissues in a TLR2/4-dependent manner. Dinoprostone 106-110 toll-like receptor 4 Mus musculus 28-32 31442584-8 2019 We hypothesized that TLR4 and its ligands repaired the epithelium after DSS-induced and radiation-induced intestinal damage by upregulating PGE2 and GM-CSF. Dinoprostone 140-144 toll-like receptor 4 Mus musculus 21-25 30665042-4 2019 Results demonstrated that RHK treatment could significantly decrease the LPS-induced production of nitric oxide, prostaglandin E2 (PGE2), interleukins (ILs) and tumour necrosis factor (TNF)-alpha in J774A.1 cells. Dinoprostone 113-129 toll-like receptor 4 Mus musculus 73-76 30665042-4 2019 Results demonstrated that RHK treatment could significantly decrease the LPS-induced production of nitric oxide, prostaglandin E2 (PGE2), interleukins (ILs) and tumour necrosis factor (TNF)-alpha in J774A.1 cells. Dinoprostone 131-135 toll-like receptor 4 Mus musculus 73-76 30056259-4 2018 The results demonstrated that nuciferine significantly inhibited LPS-induced TNF-alpha, IL-1beta, PGE2 and NO secretion. Dinoprostone 98-102 toll-like receptor 4 Mus musculus 65-68 30481583-8 2019 Interestingly, the inhibition of TLR4 signaling with CLI-095 partly inhibited NP-induced NO and PGE2 expression in BV2, a MG cell line. Dinoprostone 96-100 toll-like receptor 4 Mus musculus 33-37 30397349-0 2018 Autocrine-paracrine prostaglandin E2 signaling restricts TLR4 internalization and TRIF signaling. Dinoprostone 20-36 toll-like receptor 4 Mus musculus 57-61 30397349-3 2018 We describe a negative feedback loop driven by autocrine-paracrine prostaglandin E2 (PGE2) and the PGE2 receptor EP4 that restricted TRIF-dependent signals and the induction of interferon-beta through the regulation of TLR4 trafficking. Dinoprostone 67-83 toll-like receptor 4 Mus musculus 219-223 30397349-3 2018 We describe a negative feedback loop driven by autocrine-paracrine prostaglandin E2 (PGE2) and the PGE2 receptor EP4 that restricted TRIF-dependent signals and the induction of interferon-beta through the regulation of TLR4 trafficking. Dinoprostone 85-89 toll-like receptor 4 Mus musculus 219-223 30397349-4 2018 Inhibition of PGE2 production or antagonism of EP4 increased the rate at which TLR4 translocated to endosomes and amplified TRIF-dependent activation of the transcription factor IRF3 and caspase-8. Dinoprostone 14-18 toll-like receptor 4 Mus musculus 79-83 30397349-5 2018 This PGE2-driven mechanism restricted TLR4-TRIF signaling in vitro after infection of macrophages by the Gram-negative pathogens Escherichia coli or Citrobacter rodentium and protected mice against mortality induced by Salmonella enteritidis serovar Typhimurium. Dinoprostone 5-9 toll-like receptor 4 Mus musculus 38-42 30397349-6 2018 Thus, PGE2 restricted TLR4-TRIF signaling specifically in response to lipopolysaccharide. Dinoprostone 6-10 toll-like receptor 4 Mus musculus 22-26 30056259-7 2018 Functional aspects were analyzed using PPAR-gamma specific inhibitor GW9662, which attenuated the LPS-induced secretion of proinflammatory mediators, such as TNF-alpha, IL-1beta, PGE2, and NO. Dinoprostone 179-183 toll-like receptor 4 Mus musculus 98-101 29161659-0 2018 Lipopolysaccharide (LPS)-mediated priming of toll-like receptor 4 enhances oxidant-induced prostaglandin E2 biosynthesis in primary murine macrophages. Dinoprostone 91-107 toll-like receptor 4 Mus musculus 45-65 29712774-6 2018 Genetic deletion of 4E-BP1/2 in macrophages increased endogenous IL-10 and PGE2 protein synthesis in response to TLR4 stimulation and reduced their bactericidal capacity. Dinoprostone 75-79 toll-like receptor 4 Mus musculus 113-117 29554498-7 2018 Mg2+, especially at 5 mM, raised proliferation rates of MSCs, and modulated immune responses by decreasing levels of IL-1beta and IL-6, and by increasing levels of IL-10 and PGE2 in cells stimulated with LPS or TNF-alpha. Dinoprostone 174-178 toll-like receptor 4 Mus musculus 204-207 30233137-10 2018 Results: DCEO significantly reduced LPS-triggered production of NO and prostaglandin E2 (PGE2) and decreased protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Dinoprostone 71-87 toll-like receptor 4 Mus musculus 36-39 30233137-10 2018 Results: DCEO significantly reduced LPS-triggered production of NO and prostaglandin E2 (PGE2) and decreased protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Dinoprostone 89-93 toll-like receptor 4 Mus musculus 36-39 29161659-6 2018 In the present study, we directly tested the hypothesis that LPS-primed TLR4 will sensitize primary murine peritoneal macrophages (pM) to oxidant-mediated prostaglandin E2 (PGE2) production. Dinoprostone 155-171 toll-like receptor 4 Mus musculus 72-76 29161659-6 2018 In the present study, we directly tested the hypothesis that LPS-primed TLR4 will sensitize primary murine peritoneal macrophages (pM) to oxidant-mediated prostaglandin E2 (PGE2) production. Dinoprostone 173-177 toll-like receptor 4 Mus musculus 72-76 29161659-9 2018 In contrast, pM sensitized by prior incubation with LPS-EK, a TLR4-specific agonist, followed by oxidant stimulation exhibited increased transcriptional and translational expression of cyclooxygenase-2 (COX-2) with enhanced PGE2 biosynthesis/production only in pM derived from TLR4-WT mice but not in TLR4-KO mice. Dinoprostone 224-228 toll-like receptor 4 Mus musculus 62-66 28341741-2 2017 LPS, a TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1). Dinoprostone 52-68 toll-like receptor 4 Mus musculus 7-11 28341741-2 2017 LPS, a TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1). Dinoprostone 70-74 toll-like receptor 4 Mus musculus 7-11 26701313-4 2016 LPS increased the systemic and organ levels of proinflammatory metabolites of linoleic acid including leukotoxin diols (9-,10-DHOME, 12-,13-DHOME) and octadecadienoic acids (9-HODE and 13-HODE) and arachidonic acid-derived prostanoid, PGE2, and hydroxyeicosatetraenoic acids (8-, 12- and 15-HETE). Dinoprostone 235-239 toll-like receptor 4 Mus musculus 0-3 27788674-8 2016 In vitro, PGE2 secreted by MSCs inhibited Kupffer cell apoptosis via TLR4-ERK1/2-caspase3 pathway regulation. Dinoprostone 10-14 toll-like receptor 4 Mus musculus 69-73 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. Dinoprostone 13-17 toll-like receptor 4 Mus musculus 44-47 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. Dinoprostone 119-123 toll-like receptor 4 Mus musculus 44-47 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. Dinoprostone 119-123 toll-like receptor 4 Mus musculus 44-47 27875748-4 2017 The results showed that piperine significantly inhibited LPS-induced TNF-alpha, IL-6, IL-1beta, and PGE2 production in BV2 cells. Dinoprostone 100-104 toll-like receptor 4 Mus musculus 57-60 27569861-2 2016 BHMB concentration-dependently suppressed protein and mRNA expressions of iNOS and COX-2, thereby inhibiting the production of NO and PGE2 in LPS-stimulated RAW 264.7 cells. Dinoprostone 134-138 toll-like receptor 4 Mus musculus 142-145 27548215-5 2016 SEC or SMC suppressed LPS-induced lung expression of cyclooxygenase-2, nuclear factor-kappaB and mitogen-activated protein kinase, and lowered the generation of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin E2. Dinoprostone 229-245 toll-like receptor 4 Mus musculus 22-25 27131287-0 2016 Morin downregulates nitric oxide and prostaglandin E2 production in LPS-stimulated BV2 microglial cells by suppressing NF-kappaB activity and activating HO-1 induction. Dinoprostone 37-53 toll-like receptor 4 Mus musculus 68-71 27131287-4 2016 Morin inhibited the expression of LPS-induced proinflammatory mediators such as NO and PGE2, without any cytotoxic effects. Dinoprostone 87-91 toll-like receptor 4 Mus musculus 34-37 27131287-9 2016 Our results indicate that morin downregulates the expression of proinflammatory genes, such as iNOS and COX-2, involved in the synthesis of NO and PGE2 in LPS-stimulated BV2 microglial cells by suppressing NF-kappaB activity and activation of HO-1. Dinoprostone 147-151 toll-like receptor 4 Mus musculus 155-158 27166556-2 2016 Co-treatment with different concentrations (10, 50 and 100mug/ml) of CME was concentration-dependently reduced the LPS-induced generation of prostaglandin E2 (PGE2), nitric oxide (NO) tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6. Dinoprostone 141-157 toll-like receptor 4 Mus musculus 115-118 27166556-2 2016 Co-treatment with different concentrations (10, 50 and 100mug/ml) of CME was concentration-dependently reduced the LPS-induced generation of prostaglandin E2 (PGE2), nitric oxide (NO) tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6. Dinoprostone 159-163 toll-like receptor 4 Mus musculus 115-118 26277391-4 2015 Furthermore, the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), nitric oxide (NO) and prostaglandin E2 (PGE2) induced by LPS was inhibited by DFO in RAW264.7 macrophages. Dinoprostone 124-140 toll-like receptor 4 Mus musculus 159-162 26122137-0 2015 Prostaglandin E2 blockade enhances the pulmonary anti-Cryptococcus neoformans immune reaction via the induction of TLR-4. Dinoprostone 0-16 toll-like receptor 4 Mus musculus 115-120 26277391-4 2015 Furthermore, the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), nitric oxide (NO) and prostaglandin E2 (PGE2) induced by LPS was inhibited by DFO in RAW264.7 macrophages. Dinoprostone 142-146 toll-like receptor 4 Mus musculus 159-162 24366870-8 2014 Likewise, PGE2 production and COX2 expression were blocked in Tlr4(-/-) and Myd88(-/-) mice, but not in Cd44(-/-) mice, after LMW HA stimulation. Dinoprostone 10-14 toll-like receptor 4 Mus musculus 62-66 24495471-13 2014 CONCLUSIONS: Treatment of RAW 264.7 macrophages with a combination of PBR and LPS showed a significant concentration-dependent inhibition of nitric oxide (NO) and prostaglandin E2 (PGE2) production. Dinoprostone 163-179 toll-like receptor 4 Mus musculus 78-81 24495471-13 2014 CONCLUSIONS: Treatment of RAW 264.7 macrophages with a combination of PBR and LPS showed a significant concentration-dependent inhibition of nitric oxide (NO) and prostaglandin E2 (PGE2) production. Dinoprostone 181-185 toll-like receptor 4 Mus musculus 78-81 27057441-0 2016 TLR4 signaling promotes a COX-2/PGE2/STAT3 positive feedback loop in hepatocellular carcinoma (HCC) cells. Dinoprostone 32-36 toll-like receptor 4 Mus musculus 0-4 27057441-5 2016 Most importantly, we found a COX-2/PGE2/STAT3 positive feedback loop exists in HCC cells, which could be provoked by TLR4 activation. Dinoprostone 35-39 toll-like receptor 4 Mus musculus 117-121 27057441-9 2016 By using a primary HCC model, we observed COX-2/PGE2/STAT3 loop was significantly blocked in TLR4-/- mice compared to wild type mice, and there was no obvious tumorgenesis sign in TLR4-/- mice. Dinoprostone 48-52 toll-like receptor 4 Mus musculus 93-97 24474616-3 2014 Pretreatment of RAW 264.7 cells with THC significantly attenuated LPS-induced NO, PGE2 production, and expression of iNOS and COX-2. Dinoprostone 82-86 toll-like receptor 4 Mus musculus 66-69 24071564-2 2013 RAW264.7 cells were pretreated with piperine at 10, 50 or 100 mug/ml and subsequently stimulated with LPS (1 mug/ml) for 24 h. We found that piperine inhibited the production of prostaglandin E2 (PGE2) and nitric oxide (NO) induced by LPS. Dinoprostone 178-194 toll-like receptor 4 Mus musculus 102-105 24378351-7 2014 RESULTS: Ms-EE inhibited the production of nitric oxide (NO) and prostaglandin (PG)E2 in RAW264.7 cells and peritoneal macrophages stimulated by LPS. Dinoprostone 65-85 toll-like receptor 4 Mus musculus 145-148 22303922-10 2012 RESULTS: SPEE treatment significantly inhibited the LPS-induced production of NO, prostaglandin E(2), interleukin-6, and tumor necrosis factor-alpha and inhibited the expression of iNOS and COX-2 via attenuation of NF-kappaB p65 expression. Dinoprostone 82-100 toll-like receptor 4 Mus musculus 52-55 23665488-6 2013 We found that Rh2-B1 dramatically inhibited LPS-induced overproduction of nitric oxide, prostaglandin E2, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. Dinoprostone 88-104 toll-like receptor 4 Mus musculus 44-47 23482668-10 2013 CONCLUSION: LPS inhibit the pacemaker currents in ICCs via prostaglandin E2- and NO-dependent mechanism through toll-like receptor 4 and suggest that MAPK and NF-kappaB are implicated in these actions. Dinoprostone 59-75 toll-like receptor 4 Mus musculus 112-132 23458198-4 2013 Lipopolysaccharide (LPS) activated BV2 cells and induced the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and cytokines (interleukins-1beta and -6, and tumour necrosis factor alpha). Dinoprostone 129-145 toll-like receptor 4 Mus musculus 20-23 23458198-4 2013 Lipopolysaccharide (LPS) activated BV2 cells and induced the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and cytokines (interleukins-1beta and -6, and tumour necrosis factor alpha). Dinoprostone 147-151 toll-like receptor 4 Mus musculus 20-23 23970815-3 2013 Amentoflavone dose dependently suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW264.7 cells stimulated with the TLR4 ligand lipopolysaccharide (LPS; derived from Gram-negative bacteria). Dinoprostone 82-98 toll-like receptor 4 Mus musculus 144-148 23970815-3 2013 Amentoflavone dose dependently suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW264.7 cells stimulated with the TLR4 ligand lipopolysaccharide (LPS; derived from Gram-negative bacteria). Dinoprostone 100-104 toll-like receptor 4 Mus musculus 144-148 21073936-5 2011 We examined the effects of HC on lipopolysaccharide (LPS)-induced prostaglandin (PG) E(2) production, an indirect indicator of COX-2 activity, and COX-2 gene and protein expression in mouse peritoneal macrophages. Dinoprostone 66-89 toll-like receptor 4 Mus musculus 53-56 22380703-1 2012 AIM: The aim of the present study was to evaluate the effect of lipopolysaccharide (LPS) on the production of prostaglandin E2 (PGE2) and inhibition by nitric oxide (NO) of spontaneous contractions of uterine rings from pregnant inducible isoform of nitric oxide synthase knockout (iNOS KO) mice. Dinoprostone 110-126 toll-like receptor 4 Mus musculus 84-87 22380703-1 2012 AIM: The aim of the present study was to evaluate the effect of lipopolysaccharide (LPS) on the production of prostaglandin E2 (PGE2) and inhibition by nitric oxide (NO) of spontaneous contractions of uterine rings from pregnant inducible isoform of nitric oxide synthase knockout (iNOS KO) mice. Dinoprostone 128-132 toll-like receptor 4 Mus musculus 84-87 22380703-8 2012 RESULTS: Treatment with LPS increased PGE2 production by uterine rings from wild-type and iNOS-KO mice. Dinoprostone 38-42 toll-like receptor 4 Mus musculus 24-27 21887846-0 2011 Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonic acid-induced colitis through Cox-2 and PGE2 in a Toll-like receptor 4-dependent way. Dinoprostone 104-108 toll-like receptor 4 Mus musculus 114-134 24212947-6 2011 We have recently described two important downstream pathways underlying TLR4-mediated epithelial proliferation in a mouse model of colitis-associated cancer; i.e., cyclooxygenase 2 (COX-2)-mediated production of prostaglandin E2 (PGE2), and induction of specific ligands for epidermal growth factor receptor (EGFR). Dinoprostone 212-228 toll-like receptor 4 Mus musculus 72-76 24212947-6 2011 We have recently described two important downstream pathways underlying TLR4-mediated epithelial proliferation in a mouse model of colitis-associated cancer; i.e., cyclooxygenase 2 (COX-2)-mediated production of prostaglandin E2 (PGE2), and induction of specific ligands for epidermal growth factor receptor (EGFR). Dinoprostone 230-234 toll-like receptor 4 Mus musculus 72-76 22890360-8 2012 The inhibitory effects of LPS on ICCs were blocked by glibenclamide (an inhibitor of ATP-sensitive K(+) channels), NS-398 (a COX-2 inhibitor), AH6808 [a prostaglandin E(2) (PGE(2))-EP(2) receptor antagonist], ODQ (an inhibitor of guanylate cyclase) and L-NAME [an inhibitor of nitric oxide synthase (NOS)]. Dinoprostone 153-171 toll-like receptor 4 Mus musculus 26-29 22890360-10 2012 CONCLUSIONS: LPS can activate ICCs to release NO and PGE(2) through TLR4 activation. Dinoprostone 53-59 toll-like receptor 4 Mus musculus 13-16 22890360-10 2012 CONCLUSIONS: LPS can activate ICCs to release NO and PGE(2) through TLR4 activation. Dinoprostone 53-59 toll-like receptor 4 Mus musculus 68-72 21674704-7 2011 Villin-TLR4 mice had increased epithelial expression of COX-2 and mucosal PGE2 production at baseline. Dinoprostone 74-78 toll-like receptor 4 Mus musculus 7-11 21073936-7 2011 LPS-induced PGE(2) production was assessed by enzyme-linked immunosorbant assay and COX-2 protein expression was assessed by Western blot assay. Dinoprostone 12-18 toll-like receptor 4 Mus musculus 0-3 20688975-5 2010 PAR(2)-mediated inhibition of LPS-induced neutrophilia was mimicked by prostaglandin E(2) (PGE(2)) and butaprost [selective E-prostanoid (EP(2)) receptor agonist], and blocked by parecoxib (cyclooxygenase 2 inhibitor) and 6-isopropoxy-9-oxoxanthene-2-carboxylic acid (AH6809) (EP(1)/EP(2) receptor antagonist). Dinoprostone 71-89 toll-like receptor 4 Mus musculus 30-33 21118574-9 2010 RESULTS: We found that LPS-induced COX-2 expression and PGE2 production were mediated through NF-kappaB (p65) via activation of Toll-like receptor 4 (TLR4). Dinoprostone 56-60 toll-like receptor 4 Mus musculus 128-148 21118574-9 2010 RESULTS: We found that LPS-induced COX-2 expression and PGE2 production were mediated through NF-kappaB (p65) via activation of Toll-like receptor 4 (TLR4). Dinoprostone 56-60 toll-like receptor 4 Mus musculus 150-154 20637112-0 2010 The role of prostaglandin E2 (PGE 2) in toll-like receptor 4 (TLR4)-mediated colitis-associated neoplasia. Dinoprostone 12-28 toll-like receptor 4 Mus musculus 62-66 20637112-0 2010 The role of prostaglandin E2 (PGE 2) in toll-like receptor 4 (TLR4)-mediated colitis-associated neoplasia. Dinoprostone 30-35 toll-like receptor 4 Mus musculus 62-66 20637112-1 2010 BACKGROUND: We have previously found that TLR4-deficient (TLR4-/-) mice demonstrate decreased expression of mucosal PGE 2 and are protected against colitis-associated neoplasia. Dinoprostone 116-121 toll-like receptor 4 Mus musculus 42-46 19564573-4 2009 We found that the absence of TLR4 or TLR4-induced signaling attenuated local mucosal damage with significantly decreased cytokine and eicosanoid secretion including PGE2 production. Dinoprostone 165-169 toll-like receptor 4 Mus musculus 29-33 20018573-0 2010 Toll-like receptor 4 participates in gastric mucosal protection through Cox-2 and PGE2. Dinoprostone 82-86 toll-like receptor 4 Mus musculus 0-20 19998398-5 2010 Wogonin and NS-398, a COX-2 inhibitor, suppressed LPS-stimulated PGE(2) production in osteoblasts. Dinoprostone 65-71 toll-like receptor 4 Mus musculus 50-53 19788894-5 2009 KEY FINDINGS: Chamomile treatment inhibited the release of LPS-induced prostaglandin E(2) in RAW 264.7 macrophages. Dinoprostone 71-89 toll-like receptor 4 Mus musculus 59-62 19564573-4 2009 We found that the absence of TLR4 or TLR4-induced signaling attenuated local mucosal damage with significantly decreased cytokine and eicosanoid secretion including PGE2 production. Dinoprostone 165-169 toll-like receptor 4 Mus musculus 37-41 19564573-8 2009 Together, these data indicate that TLR4 stimulation of Cox-2 activation of PGE2 production is necessary but not sufficient for intestinal IR-induced damage and inflammation. Dinoprostone 75-79 toll-like receptor 4 Mus musculus 35-39 16849500-13 2006 Thus, LPS binds to TLR4 on osteoblasts that directly induce mPGES-1 expression for PGE(2) synthesis, leading to subsequent bone resorption. Dinoprostone 83-89 toll-like receptor 4 Mus musculus 19-23 19567393-1 2009 We previously reported that Sairei-to concentration-dependently modified lipopolysaccharide (LPS)-stimulated prostaglandin E(2) (PGE(2)) production in mouse macrophage-like RAW264.7 cells. Dinoprostone 109-127 toll-like receptor 4 Mus musculus 93-96 19567393-2 2009 Among twelve major ingredients of Sairei-to, Scutellariae radix inhibited the LPS-stimulated PGE(2) production to the greatest extent, followed by Zingiberis rhizoma, Glycyrrhizae radix, Atractylodis lanceae rhizoma and Pinelliae tuber. Dinoprostone 93-99 toll-like receptor 4 Mus musculus 78-81 19109188-0 2009 Immune complex/Ig negatively regulate TLR4-triggered inflammatory response in macrophages through Fc gamma RIIb-dependent PGE2 production. Dinoprostone 122-126 toll-like receptor 4 Mus musculus 38-42 18820644-0 2008 TLR4/MYD88-dependent, LPS-induced synthesis of PGE2 by macrophages or dendritic cells prevents anti-CD3-mediated CD95L upregulation in T cells. Dinoprostone 47-51 toll-like receptor 4 Mus musculus 0-4 18820644-8 2008 Taken together, these results indicate that APCs can regulate T-cell levels of CD95L by releasing PGE(2) in response to LPS through a TLR4/MyD88-dependent pathway, with consequences for both T cell and their own survival. Dinoprostone 98-104 toll-like receptor 4 Mus musculus 134-138 18827359-4 2008 PGE(2) production by LPS/IFN-gamma-stimulated macrophages was inhibited by APO at much lower concentrations (IC(50)=0.27 microM) than those required for the inhibition of NO production. Dinoprostone 0-6 toll-like receptor 4 Mus musculus 21-24 17673149-8 2007 We conclude that both PGE2 and VIP inhibit nitric oxide production and increase IL-10 induced by LPS in NOD macrophages and VIP effect is mediated through an increase of COX metabolites and IL-10. Dinoprostone 22-26 toll-like receptor 4 Mus musculus 97-100 19389932-9 2009 These results indicate that prostaglandin E2 signaling via either EP1 or EP2 is largely to completely necessary for Toll-like receptor 4-dependent depletion of IPCs from the SGZ and suggest further pharmacological strategies to protect this important neurogenic niche. Dinoprostone 28-44 toll-like receptor 4 Mus musculus 116-136 16952555-2 2006 We wished to test the hypothesis that cyclooxygenase 2 (Cox-2)-derived prostaglandin E2 (PGE2) is important in TLR4-related mucosal repair. Dinoprostone 71-87 toll-like receptor 4 Mus musculus 111-115 16952555-2 2006 We wished to test the hypothesis that cyclooxygenase 2 (Cox-2)-derived prostaglandin E2 (PGE2) is important in TLR4-related mucosal repair. Dinoprostone 89-93 toll-like receptor 4 Mus musculus 111-115 16952555-12 2006 PGE2 supplementation of TLR4-/- mice resulted in improvement in clinical signs of colitis and restoration of proliferation and apoptosis to WT values. Dinoprostone 0-4 toll-like receptor 4 Mus musculus 24-28 16536595-8 2006 In addition, CL-bromelain dose-dependently inhibited LPS-induced COX-2 mRNA and prostaglandin E2 (PGE2) in BV-2 microglial cells. Dinoprostone 80-96 toll-like receptor 4 Mus musculus 53-56 16536595-8 2006 In addition, CL-bromelain dose-dependently inhibited LPS-induced COX-2 mRNA and prostaglandin E2 (PGE2) in BV-2 microglial cells. Dinoprostone 98-102 toll-like receptor 4 Mus musculus 53-56 14527510-3 2003 This study is the first report on the inhibition by prostaglandin E2 (PGE2) of TNF release from bone marrow-derived dendritic cells stimulated with lipopolysaccharide (LPS), a TLR4 ligand, or peptidoglycan, a TLR2 ligand. Dinoprostone 52-68 toll-like receptor 4 Mus musculus 176-180 16276975-3 2005 This compound inhibited LPS-induced nitric oxide (NO) or prostaglandin (PG) E2 production in dose-dependent manners, with IC50 values of 7.2 microM and 5.3 microM, respectively. Dinoprostone 57-78 toll-like receptor 4 Mus musculus 24-27 16038627-6 2005 The LPS-induced increases in the release of PGE2, NO, TNF-alpha and IL-1beta from macrophages were attenuated by pre-treatment with celecoxib. Dinoprostone 44-48 toll-like receptor 4 Mus musculus 4-7 15546960-5 2005 In response to LPS, COX-2 expression and PGE2 production increased by two- to four-fold, which were completely blocked by a selective COX-2 inhibitor NS398. Dinoprostone 41-45 toll-like receptor 4 Mus musculus 15-18 15546960-7 2005 Deficiency of gp91(phox) or suppression of p22(phox) expression decreased NADH oxidase activity and down-regulated COX-2 expression and PGE2 production stimulated by LPS. Dinoprostone 136-140 toll-like receptor 4 Mus musculus 166-169 15546960-8 2005 Pharmacological inhibitors of NADH oxidase prevented LPS-induced COX-2 expression and PGE2 production. Dinoprostone 86-90 toll-like receptor 4 Mus musculus 53-56 14527510-3 2003 This study is the first report on the inhibition by prostaglandin E2 (PGE2) of TNF release from bone marrow-derived dendritic cells stimulated with lipopolysaccharide (LPS), a TLR4 ligand, or peptidoglycan, a TLR2 ligand. Dinoprostone 70-74 toll-like receptor 4 Mus musculus 176-180 12529332-1 2003 We have shown that the age-associated increase in lipopolysaccharide (LPS)-stimulated macrophages (M phi) prostaglandin E(2) (PGE(2)) production is because of ceramide-induced up-regulation of cyclooxygenase (COX)-2 transcription that leads to increased COX-2 expression and enzyme activity. Dinoprostone 106-124 toll-like receptor 4 Mus musculus 70-73 12834283-4 2003 Further, while (-)-epigallocatechin gallate (EGCG) alone increased LPS/IFM-gamma-induced production of PGE2 and TNF-alpha as well as cyclooxygenase-2 expression, the EGCG/GEN combination markedly suppressed these parameters. Dinoprostone 103-107 toll-like receptor 4 Mus musculus 67-70 12023384-0 2002 Lipopolysaccharide-dependent prostaglandin E(2) production is regulated by the glutathione-dependent prostaglandin E(2) synthase gene induced by the Toll-like receptor 4/MyD88/NF-IL6 pathway. Dinoprostone 29-47 toll-like receptor 4 Mus musculus 149-169 12177064-3 2002 In RON-expressing macrophages treated with macrophage stimulating protein, LPS-induced prostaglandin E(2) (PGE(2)) production was significantly reduced. Dinoprostone 87-105 toll-like receptor 4 Mus musculus 75-78 12177064-3 2002 In RON-expressing macrophages treated with macrophage stimulating protein, LPS-induced prostaglandin E(2) (PGE(2)) production was significantly reduced. Dinoprostone 107-113 toll-like receptor 4 Mus musculus 75-78 12072440-1 2002 Previously, we showed that macrophages (MO) from old mice have significantly higher levels of lipopolysaccharide (LPS)-induced prostaglandin E(2) (PGE(2)) production than young mice, due to increased cyclooxygenase-2 (COX-2) mRNA levels. Dinoprostone 127-145 toll-like receptor 4 Mus musculus 114-117 12072440-5 2002 The addition of ceramide in the presence or absence of LPS resulted in a significant increase in PGE(2) production in a dose- and time-dependent manner. Dinoprostone 97-103 toll-like receptor 4 Mus musculus 55-58 11239502-4 2001 Ajoene was shown to dose-dependently inhibit the release of LPS (1 microg/mL)-induced prostaglandin E(2) in RAW 264.7 macrophages (IC(50) value: 2.4 microM). Dinoprostone 86-104 toll-like receptor 4 Mus musculus 60-63 11272279-5 2001 LPS alone triggered the release of PGE2, TNF-alpha, and IL-6; all of which were potentiated by the presence of TG, but not of UTP. Dinoprostone 35-39 toll-like receptor 4 Mus musculus 0-3 11272279-7 2001 PGE2, TNF-alpha, and IL-6 release by LPS alone were attenuated by Ro 31-8220, Go6976, PD 098059, SB 203580, and PDTC. Dinoprostone 0-4 toll-like receptor 4 Mus musculus 37-40 10545778-1 1999 Our previous study has demonstrated the potentiation by uridine triphosphate (UTP) of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production in lipopolysaccharide (LPS)-stimulated murine J774 macrophages. Dinoprostone 108-126 toll-like receptor 4 Mus musculus 170-173 9887177-4 1999 The hypothermic effect of LPS was accompanied by a significant elevation in TNF-alpha level in plasma and in LT and PGE2 production by ex vivo-incubated hypothalamus. Dinoprostone 116-120 toll-like receptor 4 Mus musculus 26-29 7766705-3 1995 The COX2 expression was amplified by arachidonic acid cascade stimulating agents (Ca, Mg, zymosan) and by LPS in a time-dependant manner; PGE2 by itself amplified LPS-induced COX2 expression. Dinoprostone 138-142 toll-like receptor 4 Mus musculus 106-109 7766705-3 1995 The COX2 expression was amplified by arachidonic acid cascade stimulating agents (Ca, Mg, zymosan) and by LPS in a time-dependant manner; PGE2 by itself amplified LPS-induced COX2 expression. Dinoprostone 138-142 toll-like receptor 4 Mus musculus 163-166