PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
31568781-8	2019	We found that: nalbuphine (a) antagonized scratching in a dose- and time-dependent manner without affecting locomotion, b) decreased IL-31, and increased anti-inflammatory IL-10, and c) induced more elevations in the levels of CCL2, CCL3, CCL12, CXCL1, CXCL2, CXCL9, CXCL10, IL-1beta, IL-16, TIMP-1, M-CSF, TREM-1 and M1-type macrophages compared to saline.	Nalbuphine	15-25	interleukin 16	Mus musculus	285-290
32524776-5	2020	Interestingly, we observed distinct large bright CD11b positive cells in the bronchoalveolar lavage, upregulation of lung vascular and alveolar ATP synthase as well as plasminogen and bronchiolar angiostatin expression in ozone-exposed mice, platelet and neutrophil accumulation in the lung vasculature and an eotaxin-2, IL-16, CXCL5, CXCL12, and CXCL13 dominant inflammatory response leading to lung injury.	Ozone	222-227	interleukin 16	Mus musculus	321-326
31940604-7	2019	RESULTS: In the brain of HFD-fed mice, levels of the proinflammatory cytokines interleukin 16 and tumor necrosis factor alpha were reduced by donepezil treatment.	donepezil	142-151	interleukin 16	Mus musculus	79-125
30738184-4	2019	Application of recombinant IL-16 impairs both glutamate-induced increases in intracellular Ca2+ and sEPSC frequency and amplitude in a CD4- and CD9-independent manner.	Glutamic Acid	46-55	interleukin 16	Mus musculus	27-32
28527399-6	2017	The co-administration of melamine and cyanuric acid with high dose (each at 16mgkg-12d-1) led to a significantly lower contents of IL-10, IL-16 and monocyte chemoattractant protein-1 (MCP-1) in mouse serum in comparison to negative control group.	melamine	25-33	interleukin 16	Mus musculus	138-143
30384867-14	2018	Compared with WT DSS treatment group, IL-16-/- DSS treatment group showed less changes in body mass, less colon tissue damage, and markedly lower percents of apoptotic cells in the peritoneal or colonic tissues of IL-16-/- mice.	Dextran Sulfate	47-50	interleukin 16	Mus musculus	38-43
30384867-14	2018	Compared with WT DSS treatment group, IL-16-/- DSS treatment group showed less changes in body mass, less colon tissue damage, and markedly lower percents of apoptotic cells in the peritoneal or colonic tissues of IL-16-/- mice.	Dextran Sulfate	47-50	interleukin 16	Mus musculus	214-219
30384867-15	2018	What"s more, the number of macrophages, the polarization level of M1 macrophages, and the levels of the iconic inflammatory factors IL-6 and IL-12 significantly decreased in IL-16-/- DSS treatment group compared with WT DSS treatment group.	Dextran Sulfate	183-186	interleukin 16	Mus musculus	174-179
30384867-15	2018	What"s more, the number of macrophages, the polarization level of M1 macrophages, and the levels of the iconic inflammatory factors IL-6 and IL-12 significantly decreased in IL-16-/- DSS treatment group compared with WT DSS treatment group.	Dextran Sulfate	220-223	interleukin 16	Mus musculus	174-179
30384867-16	2018	Conclusion IL-16 can aggravate DSS-induced IBD by promoting the polarization of M1 macrophages.	Dextran Sulfate	31-34	interleukin 16	Mus musculus	11-16
30089723-5	2018	Neutrophil infiltration was markedly reduced in the peritoneal lavage of pristane-treated IL-16-deficient mice and elevated following i.n.	pristane	73-81	interleukin 16	Mus musculus	90-95
30384867-0	2018	[IL-16 aggravates dextran sulfate sodium (DSS)-induced mouse inflammatory bowel disease by promoting M1 polarization of macrophages].	Dextran Sulfate	18-40	interleukin 16	Mus musculus	1-6
30384867-0	2018	[IL-16 aggravates dextran sulfate sodium (DSS)-induced mouse inflammatory bowel disease by promoting M1 polarization of macrophages].	Dextran Sulfate	42-45	interleukin 16	Mus musculus	1-6
30384867-13	2018	Results DSS induced high expression of IL-16 in the colon tissue.	Dextran Sulfate	8-11	interleukin 16	Mus musculus	39-44
30384867-14	2018	Compared with WT DSS treatment group, IL-16-/- DSS treatment group showed less changes in body mass, less colon tissue damage, and markedly lower percents of apoptotic cells in the peritoneal or colonic tissues of IL-16-/- mice.	Dextran Sulfate	17-20	interleukin 16	Mus musculus	38-43
28527399-6	2017	The co-administration of melamine and cyanuric acid with high dose (each at 16mgkg-12d-1) led to a significantly lower contents of IL-10, IL-16 and monocyte chemoattractant protein-1 (MCP-1) in mouse serum in comparison to negative control group.	cyanuric acid	38-51	interleukin 16	Mus musculus	138-143
26370374-6	2015	In mouse cytokine array measuring 40 cytokines, the productions of interleukin-16, TIMP-1, and tumor necrosis factor-alpha (TNF-alpha) were significantly reduced with 0.1 mug/mL of rivaroxaban pretreatment (all P < 0.05).	Rivaroxaban	181-192	interleukin 16	Mus musculus	67-81
28193233-8	2017	Placental production of TNFalphaand IL16 in the tacrolimus-treated HFD-dNONcNZO dams were restored to non-diabetic levels and the treatment resulted in the inhibition of aberrant monocyte/macrophage activation during pregnancy in the HFD-dNONcNZO dams.	Tacrolimus	48-58	interleukin 16	Mus musculus	36-40
28193233-8	2017	Placental production of TNFalphaand IL16 in the tacrolimus-treated HFD-dNONcNZO dams were restored to non-diabetic levels and the treatment resulted in the inhibition of aberrant monocyte/macrophage activation during pregnancy in the HFD-dNONcNZO dams.	dnoncnzo	71-79	interleukin 16	Mus musculus	36-40
28193233-8	2017	Placental production of TNFalphaand IL16 in the tacrolimus-treated HFD-dNONcNZO dams were restored to non-diabetic levels and the treatment resulted in the inhibition of aberrant monocyte/macrophage activation during pregnancy in the HFD-dNONcNZO dams.	dnoncnzo	238-246	interleukin 16	Mus musculus	36-40
27037906-8	2016	We show that bortezomib promotes pro-inflammatory macrophages which account for MM cell aggressiveness, an effect which is partially mediated by interleukin-16.	Bortezomib	13-23	interleukin 16	Mus musculus	145-159
25551570-9	2014	Instillation of bleomycin but not Ad increased the expression of IL-1alpha, IL-13 and IL-16.	Bleomycin	16-25	interleukin 16	Mus musculus	86-91
22959056-7	2013	In addition, we found that EGCG prevented LPS-induced activation of astrocytes and elevation of cytokines including tumor necrosis factor-alpha, interleukin (IL)-1beta, macrophage colony-stimulating factor, soluble intercellular adhesion molecule-1 and IL-16, and the increase of inflammatory proteins, such as inducible nitric oxide synthase and cyclooxygenase-2, which are known factors responsible for not only activation of astrocytes but also amyloidogenesis.	epigallocatechin gallate	27-31	interleukin 16	Mus musculus	253-258
24310731-3	2014	Our results indicated that atRA and retinol could induce GM-CSF and IL-16 expression, whereas all these tested substances enhanced MMP-9 production.	Tretinoin	27-31	interleukin 16	Mus musculus	68-73
24310731-3	2014	Our results indicated that atRA and retinol could induce GM-CSF and IL-16 expression, whereas all these tested substances enhanced MMP-9 production.	Vitamin A	36-43	interleukin 16	Mus musculus	68-73
24310731-5	2014	AtRA and retinol affected GM-CSF and IL-16 expression mainly through RA receptor beta (RARbeta).	Tretinoin	0-4	interleukin 16	Mus musculus	37-42
24310731-5	2014	AtRA and retinol affected GM-CSF and IL-16 expression mainly through RA receptor beta (RARbeta).	Vitamin A	9-16	interleukin 16	Mus musculus	37-42
24310731-10	2014	Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity.	Tretinoin	65-69	interleukin 16	Mus musculus	130-135
24310731-10	2014	Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity.	Vitamin A	71-78	interleukin 16	Mus musculus	130-135
24310731-10	2014	Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity.	beta Carotene	84-97	interleukin 16	Mus musculus	130-135
23768053-9	2013	Numerous genes were up- or down-regulated by more than twofold by steroid treatment, including proinflammatory interleukins (IL-16) and anti-inflammatory cytokines.	Steroids	66-73	interleukin 16	Mus musculus	125-130
21622115-4	2011	Costunolide attenuated the expression of tumour necrosis factor-alpha, interleukin-1,6, inducible nitric oxide synthase, monocyte chemotactic protein 1 and cyclooxygenase 2 in activated microglia.	costunolide	0-11	interleukin 16	Mus musculus	71-119
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Creatinine	136-146	interleukin 16	Mus musculus	16-21
19232499-6	2009	Our current study demonstrates that IL-16, and its activator caspase 3, are highly expressed at the mRNA level in the lungs of mice prior to the deposition of collagen following intratracheal bleomycin administration.	Bleomycin	192-201	interleukin 16	Mus musculus	36-41
19295235-4	2009	OBJECTIVE: We evaluated the variability of IL-16 and the effects of the antiallergic drugs fexofenadine (40 mg/kg/day) and ramatroban (30 mg/kg/day) on IL-16 in an OVA-sensitized BALB/c murine experimental allergic rhinitis model.	fexofenadine	91-103	interleukin 16	Mus musculus	152-157
19295235-4	2009	OBJECTIVE: We evaluated the variability of IL-16 and the effects of the antiallergic drugs fexofenadine (40 mg/kg/day) and ramatroban (30 mg/kg/day) on IL-16 in an OVA-sensitized BALB/c murine experimental allergic rhinitis model.	ramatroban	123-133	interleukin 16	Mus musculus	152-157
19295235-8	2009	Fexofenadine and ramatroban significantly inhibited the following OVA-induced allergic features when compared to the nontreated sensitized group: sneezing, nasal rubbing, eosinophil infiltration, IL-16 expressions in nasal tissue, and serum IL-16 level.	fexofenadine	0-12	interleukin 16	Mus musculus	196-201
19295235-8	2009	Fexofenadine and ramatroban significantly inhibited the following OVA-induced allergic features when compared to the nontreated sensitized group: sneezing, nasal rubbing, eosinophil infiltration, IL-16 expressions in nasal tissue, and serum IL-16 level.	fexofenadine	0-12	interleukin 16	Mus musculus	241-246
19295235-8	2009	Fexofenadine and ramatroban significantly inhibited the following OVA-induced allergic features when compared to the nontreated sensitized group: sneezing, nasal rubbing, eosinophil infiltration, IL-16 expressions in nasal tissue, and serum IL-16 level.	ramatroban	17-27	interleukin 16	Mus musculus	196-201
19295235-8	2009	Fexofenadine and ramatroban significantly inhibited the following OVA-induced allergic features when compared to the nontreated sensitized group: sneezing, nasal rubbing, eosinophil infiltration, IL-16 expressions in nasal tissue, and serum IL-16 level.	ramatroban	17-27	interleukin 16	Mus musculus	241-246
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Creatinine	136-146	interleukin 16	Mus musculus	45-50
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Urea	156-160	interleukin 16	Mus musculus	16-21
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Urea	156-160	interleukin 16	Mus musculus	45-50
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Nitrogen	161-169	interleukin 16	Mus musculus	16-21
18004294-6	2008	Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice.	Nitrogen	161-169	interleukin 16	Mus musculus	45-50
12594062-6	2003	The mechanism for IL-16 production was shown to be caspase-3-dependent, and serotonin-induced secretion of IL-16 required binding of the serotonin type 2 receptor.	Serotonin	76-85	interleukin 16	Mus musculus	107-112
15807844-4	2005	IL-16 production was induced in the epidermis and dermis during the elicitation phase of the CHS response with trinitrochlorobenzene.	Picryl Chloride	111-132	interleukin 16	Mus musculus	0-5
15807844-5	2005	In the sensitization phase, the single application of haptens such as trinitrochlorobenzene and oxazolone also induced IL-16, whereas primary irritants or vehicle control did not.	Picryl Chloride	70-91	interleukin 16	Mus musculus	119-124
15807844-5	2005	In the sensitization phase, the single application of haptens such as trinitrochlorobenzene and oxazolone also induced IL-16, whereas primary irritants or vehicle control did not.	Oxazolone	96-105	interleukin 16	Mus musculus	119-124
15728482-3	2005	Consistent with the microarray reports, pro-IL-16 mRNA levels fell within 4 h of activation, and this response is inhibited by cyclosporin A.	Cyclosporine	127-140	interleukin 16	Mus musculus	44-49
15728482-7	2005	Stimulation with anti-CD3 mAb induced transiently greater thymidine incorporation in IL-16-deficient CD4(+) T cells than wild-type controls, but there was no difference in cell survival or in the CFSE dilution profiles.	Thymidine	58-67	interleukin 16	Mus musculus	85-90
12594062-0	2003	Tumor necrosis factor-alpha-induced synthesis of interleukin-16 in airway epithelial cells: priming for serotonin stimulation.	Serotonin	104-113	interleukin 16	Mus musculus	49-63
12594062-2	2003	IL-16 is only present in the bronchoalveolar lavage (BAL) fluid following airway challenge with either allergen or vasoactive amine.	Amines	126-131	interleukin 16	Mus musculus	0-5
12594062-7	2003	The relevance of the priming effect associated with sensitization for IL-16 production and storage was confirmed in vivo by serotonin airway challenge of OVA-sensitized mice, resulting in rapid secretion of IL-16 into BAL fluid.	Serotonin	124-133	interleukin 16	Mus musculus	70-75
12594062-5	2003	We determined that ovalbumin (OVA)-sensitized mice have an increase in systemic tumor necrosis factor-alpha levels, and that serum or BAL fluid stimulation of bronchial epithelial cells results in production of IL-16 that is subsequently secreted only following serotonin stimulation.	Serotonin	262-271	interleukin 16	Mus musculus	211-216
12594062-7	2003	The relevance of the priming effect associated with sensitization for IL-16 production and storage was confirmed in vivo by serotonin airway challenge of OVA-sensitized mice, resulting in rapid secretion of IL-16 into BAL fluid.	Serotonin	124-133	interleukin 16	Mus musculus	207-212
11086073-7	2000	Using murine T cell hybridomas transfected to express native or mutated forms of CD4, it was determined that IL-16/CD4 induces a p56(lck)-dependent inhibitory signal for CXCR4, which is independent of its tyrosine catalytic activity.	Tyrosine	205-213	interleukin 16	Mus musculus	109-114
33958974-0	2021	Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice.	Doxorubicin	113-124	interleukin 16	Mus musculus	5-19
10479680-11	1999	Exposure of these cells to IL-16 induces expression of the immediate-early gene, c-fos, via a signaling pathway that involves tyrosine phosphorylation.	Tyrosine	126-134	interleukin 16	Mus musculus	27-32
34071825-4	2021	Our data show that IL-16 expression is significantly increased in the brain and spinal cord tissues of EAE mice compared to phosphate buffered saline (PBS) immunised controls.	pbs	151-154	interleukin 16	Mus musculus	19-24
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interleukin 16	Mus musculus	98-112
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	CUDC-907	167-175	interleukin 16	Mus musculus	113-118
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	TMP195	180-187	interleukin 16	Mus musculus	98-112
35291899-10	2022	Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195.	TMP195	180-187	interleukin 16	Mus musculus	113-118
35502244-10	2022	In cultured alveolar macrophages, Dex reduced LPS-mediated expression of IL-1, -6 and TNF-alpha receptors while promoting alveolar macrophages differentiation towards a M2 anti-inflammatory phenotype.	Dexmedetomidine	34-37	interleukin 16	Mus musculus	73-81
33958974-12	2021	Conclusions: The anti-IL-16 nAb protects against DOX-induced cardiac injury by reducing cardiac inflammation, and IL-16 may be a promising target to prevent DOX-related cardiac injury.	Doxorubicin	49-52	interleukin 16	Mus musculus	22-27
33958974-12	2021	Conclusions: The anti-IL-16 nAb protects against DOX-induced cardiac injury by reducing cardiac inflammation, and IL-16 may be a promising target to prevent DOX-related cardiac injury.	Doxorubicin	157-160	interleukin 16	Mus musculus	114-119
11040184-3	2000	The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice.	Trinitrobenzenesulfonic Acid	141-170	interleukin 16	Mus musculus	119-124
11040184-3	2000	The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice.	Trinitrobenzenesulfonic Acid	172-176	interleukin 16	Mus musculus	119-124
11040184-8	2000	Anti-IL-16 mAb treatment significantly reduced TNBS-induced weight loss (P< 0.001), mucosal ulceration (P<0.05), myeloperoxidase activity (P< 0.001), and TNBS-mediated increases in mucosal levels of IL-1beta (P<0.05) and tumor necrosis factor alpha (P<0.01).	Trinitrobenzenesulfonic Acid	47-51	interleukin 16	Mus musculus	5-10
11040184-9	2000	CONCLUSIONS: Anti-IL-16 mAb reduced colonic injury and inflammation induced by TNBS in mice.	Trinitrobenzenesulfonic Acid	79-83	interleukin 16	Mus musculus	18-23
35530977-0	2022	Corrigendum to "Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice".	Doxorubicin	129-140	interleukin 16	Mus musculus	21-35
33958974-3	2021	In this study, the role of IL-16 in DOX-induced cardiac injury and the possible mechanisms were examined.	Doxorubicin	36-39	interleukin 16	Mus musculus	27-32
33958974-4	2021	Methods: Cardiac IL-16 levels were first measured in DOX- or saline-treated mice.	Doxorubicin	53-56	interleukin 16	Mus musculus	17-22
33958974-8	2021	Results: DOX administration increased IL-16 expression in cardiac macrophages compared with that of saline treatment.	Doxorubicin	9-12	interleukin 16	Mus musculus	38-43
33958974-9	2021	The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice.	nab	15-18	interleukin 16	Mus musculus	9-14
33958974-9	2021	The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice.	Doxorubicin	193-196	interleukin 16	Mus musculus	9-14
33958974-11	2021	In cell studies, the anti-IL-16 nAb also reduced DOX-induced M1 macrophage differentiation and alleviated apoptosis in cardiomyocytes cocultured with macrophages.	nab	32-35	interleukin 16	Mus musculus	26-31
33958974-11	2021	In cell studies, the anti-IL-16 nAb also reduced DOX-induced M1 macrophage differentiation and alleviated apoptosis in cardiomyocytes cocultured with macrophages.	Doxorubicin	49-52	interleukin 16	Mus musculus	26-31
33958974-12	2021	Conclusions: The anti-IL-16 nAb protects against DOX-induced cardiac injury by reducing cardiac inflammation, and IL-16 may be a promising target to prevent DOX-related cardiac injury.	nab	28-31	interleukin 16	Mus musculus	22-27
33628366-8	2021	Additionally, treatment with CPUY192018, the nuclear factor erythroid-2 related factor 2 (Nrf2) pathway, significantly increased mortality and reversed the above effects in mice treated with LPS and the anti-IL-16 nAb.	CPUY013 compound	29-39	interleukin 16	Mus musculus	208-213