PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17169865-2 2007 We have recently reported that early changes in NO2-exposed human bronchial epithelial cells are causally linked to increased generation of proinflammatory mediators, such as nitric oxide/nitrite and cytokines like interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-8. Nitrogen Dioxide 48-51 tumor necrosis factor Homo sapiens 239-272 15003325-8 2004 Furthermore, a significant increase in IL-1beta and TNF-alpha generation was observed in the NO2-exposed cells. Nitrogen Dioxide 93-96 tumor necrosis factor Homo sapiens 52-61 12451238-7 2002 Moreover, although TNF-alpha levels were significantly raised in HTx recipients compared with both healthy controls and individuals with essential hypertension, it was positively correlated to 24-hour BP and NO2(-) + NO3(-). Nitrogen Dioxide 208-211 tumor necrosis factor Homo sapiens 19-28 11103793-9 2000 When combined with IFN-gamma, the recombinant TNF-alpha (1-100 ng/ml) enhanced NO2- formation in JB6 P+ cells, whereas IL-1beta (1-100 ng/ml) did not. Nitrogen Dioxide 79-82 tumor necrosis factor Homo sapiens 46-55 11360609-6 1999 In endothelium culture supernatant with TNF-alpha group, synthesis of ET-1, NO2- and 6-ket-PGF1 alpha increased, expression of FN on the surface of endothelial cells decreased, white blood cells adhesion to endothelial cells increased. Nitrogen Dioxide 76-79 tumor necrosis factor Homo sapiens 40-49 10066641-8 1999 We observed an increased IL-1beta-, IL-6-, IL-8- and TNF-alpha-specific mRNA expression of particle or fibre exposed AM, which was decreased after an additional NO2 exposure. Nitrogen Dioxide 161-164 tumor necrosis factor Homo sapiens 53-62 10066641-9 1999 Also the particle or fibre exposure induced significant increase in IL-1beta-, IL-6-, IL-8 and TNF-alpha-release of AM which was decreased after an additional NO2 exposure (p <0.031). Nitrogen Dioxide 159-162 tumor necrosis factor Homo sapiens 95-104 9176264-4 1997 PAEM were incubated with TNF-alpha (100 U/ml) for 4 h. Incubation of PAEM with TNF-alpha resulted in increases in 1) the .NO oxidation product nitrite (NO2-), 2) nitrotyrosine immunofluorescence, 3) the oxidation of p42 (tentatively identified as actin), and 4) permeability to Evans blue dye-albumin. Nitrogen Dioxide 152-155 tumor necrosis factor Homo sapiens 25-34 9176264-4 1997 PAEM were incubated with TNF-alpha (100 U/ml) for 4 h. Incubation of PAEM with TNF-alpha resulted in increases in 1) the .NO oxidation product nitrite (NO2-), 2) nitrotyrosine immunofluorescence, 3) the oxidation of p42 (tentatively identified as actin), and 4) permeability to Evans blue dye-albumin. Nitrogen Dioxide 152-155 tumor necrosis factor Homo sapiens 79-88 9176264-5 1997 The .NO synthase inhibitor aminoguanidine (100 microM) prevented the TNF-alpha-induced increase in NO2-, nitrotyrosine immunofluorescence, oxidized p42, and permeability. Nitrogen Dioxide 99-102 tumor necrosis factor Homo sapiens 69-78 10072993-2 1997 The results showed that the concentration of NO2-/NO3- and the levels of TNF-alpha and IL-8 in CSF of the two kinds of meningitis were higher than those of normal CSF, and the concentration of NO2-/NO3- correlated positively to the content of TNF-alpha. Nitrogen Dioxide 193-196 tumor necrosis factor Homo sapiens 243-252 9812557-5 1997 The concentration of NO2-/NO3- had a positive correlation with that of endotoxin and TNF alpha (r = 0.481, P < 0.01; r = 0.351, P < 0.05). Nitrogen Dioxide 21-24 tumor necrosis factor Homo sapiens 71-94 8747002-0 1996 Modulation of IL-1 beta, IL-6, IL-8, TNF-alpha, and TGF-beta secretions by alveolar macrophages under NO2 exposure. Nitrogen Dioxide 102-105 tumor necrosis factor Homo sapiens 37-46 8747002-7 1996 Exposure for 30 min to NO2 induced a significant decrease of LPS-stimulated IL-1 Beta, IL-6, IL-8, and TNF-alpha (p < .05). Nitrogen Dioxide 23-26 tumor necrosis factor Homo sapiens 103-112 8747002-10 1996 NO2 exposure of LPS-stimulated AM resulted in a functional impairment of AM after NO2 exposure regarding IL-1 beta, IL-6, IL-8, and TNF-alpha. Nitrogen Dioxide 0-3 tumor necrosis factor Homo sapiens 132-141 7510778-6 1994 This is confirmed by the finding that the culture supernatants of N103 cells induced by TNF-alpha and IFN-gamma, but not that by IL-6, contained high levels of NO2-, the production of which was inhibited by L-NG-monomethylarginine. Nitrogen Dioxide 160-163 tumor necrosis factor Homo sapiens 88-97 7688311-4 1993 IL-10 further increased NO2- production by M phi stimulated in the presence of optimal concentrations of prostaglandin E2, a positive modulator of M phi activation by IFN-gamma/TNF-alpha. Nitrogen Dioxide 24-27 tumor necrosis factor Homo sapiens 177-186 1658153-5 1991 A combination of IL-1, LPS, and TNF-alpha was shown to induce maximal production of 355 +/- 51 nmol/10(6) cells/72 h of nitrite (NO2-), which was measured as a stable end-product of .N = O generation. Nitrogen Dioxide 129-132 tumor necrosis factor Homo sapiens 32-41 34634403-9 2022 Meanwhile, a 10 mug/m3 increase in NO2 was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-alpha. Nitrogen Dioxide 35-38 tumor necrosis factor Homo sapiens 106-115 34879788-4 2021 Generalized estimating equation was used to evaluate the association between exposure to PM2.5 and NO2 and the following serum cytokine levels on the 7 days preceding clinical assessment and serum collection: MCP1, IL-6, IL-8, IL-10, IL-17, IFN-alpha, and TNF-alpha. Nitrogen Dioxide 99-102 tumor necrosis factor Homo sapiens 256-265 25912222-7 2015 Endogenous TNFalpha neutralization with an anti-TNFalpha monoclonal antibody (mAb) successfully inhibited NO2(-) synthesis by blood mononuclear cells and tumor explants. Nitrogen Dioxide 106-110 tumor necrosis factor Homo sapiens 11-19 25912222-7 2015 Endogenous TNFalpha neutralization with an anti-TNFalpha monoclonal antibody (mAb) successfully inhibited NO2(-) synthesis by blood mononuclear cells and tumor explants. Nitrogen Dioxide 106-110 tumor necrosis factor Homo sapiens 48-56 25912222-8 2015 Recombinant TNFalpha (rTNFalpha) enhanced NO2(-) synthesis and C666-1 NPC cell proliferation. Nitrogen Dioxide 42-45 tumor necrosis factor Homo sapiens 12-20 25912222-9 2015 NOS2 selective inhibition (1400W) and TNFalpha antagonization with an anti-TNFalpha mAb potently inhibited rTNFalpha induced C666-1 proliferation and NO2(-) production. Nitrogen Dioxide 150-153 tumor necrosis factor Homo sapiens 38-46 25912222-9 2015 NOS2 selective inhibition (1400W) and TNFalpha antagonization with an anti-TNFalpha mAb potently inhibited rTNFalpha induced C666-1 proliferation and NO2(-) production. Nitrogen Dioxide 150-153 tumor necrosis factor Homo sapiens 75-83 25912222-11 2015 Altogether, our results define monocytes/macrophages and the primary tumor as major sources of circulating NO2(-) in NPC patients and support the idea that antibody dependent inhibition of the TNFalpha/NOS2 pathway may alter NPC tumor growth. Nitrogen Dioxide 107-110 tumor necrosis factor Homo sapiens 193-201 24243740-8 2014 TNFA -308G>A modified the action of ozone and nitrogen dioxide on lung function, asthma risk, and symptoms; however, the direction of association varied between studies. Nitrogen Dioxide 49-65 tumor necrosis factor Homo sapiens 0-4