PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21506877-7 2011 Both NO2 (25 ppm) and DEP gave lung damage, measured as increased total protein concentration in BALF, whereas only NO2 seemed to stimulate release of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha). Nitrogen Dioxide 116-119 tumor necrosis factor Mus musculus 180-207 21506877-7 2011 Both NO2 (25 ppm) and DEP gave lung damage, measured as increased total protein concentration in BALF, whereas only NO2 seemed to stimulate release of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha). Nitrogen Dioxide 116-119 tumor necrosis factor Mus musculus 209-218 18236232-11 2008 Instead, NO2 exposure attenuated the smoke-induced increases in levels of TNF-alpha, KC, and MCP-1. Nitrogen Dioxide 9-12 tumor necrosis factor Mus musculus 74-83 8228620-5 1993 Interestingly, when macrophages were pretreated with TGF-beta for 24 h, NO2- production in response to IFN-gamma plus TNF-alpha was also inhibited. Nitrogen Dioxide 72-75 tumor necrosis factor Mus musculus 118-127 11103793-8 2000 The addition of IFN-gamma-treated RAW 264.7 cell-conditioned media to P+ subclones led to a significant enhancement of NO2- formation that was diminished by the TNF-alpha-specific but not IL-1beta-specific antibody. Nitrogen Dioxide 119-122 tumor necrosis factor Mus musculus 161-170 9712914-5 1998 Antibody-mediated blockade of CD120a (p55) completely inhibited NO2- expression in response to TNFalpha, whereas blockade of CD120b (p75) reduced NO2- accumulation by approximately 50%. Nitrogen Dioxide 64-67 tumor necrosis factor Mus musculus 95-103 8003032-2 1994 TNF alpha, IL-1 beta, and LPS caused a dose- and time-dependent increase of nitrite (NO2-), the stable metabolite of nitric oxide (NO), in conditioned media over 48 hours, while IFN gamma had a minimal effect. Nitrogen Dioxide 85-88 tumor necrosis factor Mus musculus 0-9 9586818-11 1998 TNFalpha and LPS both increased NO2 in GPTE cells, but none of the Ca++-mobilizing agents nor p + XO significantly affected intracellular RNS. Nitrogen Dioxide 32-35 tumor necrosis factor Mus musculus 0-8 9192827-7 1997 Experiments designed to investigate the role of tumor necrosis factor alpha (TNF-alpha) in NO2- production by Bryo- and IFN-gamma-activated macrophages revealed that ANA-1 macrophages expressed low levels of TNF-alpha mRNA constitutively that were not augmented in the presence of IFN-gamma. Nitrogen Dioxide 91-94 tumor necrosis factor Mus musculus 48-75 9192827-7 1997 Experiments designed to investigate the role of tumor necrosis factor alpha (TNF-alpha) in NO2- production by Bryo- and IFN-gamma-activated macrophages revealed that ANA-1 macrophages expressed low levels of TNF-alpha mRNA constitutively that were not augmented in the presence of IFN-gamma. Nitrogen Dioxide 91-94 tumor necrosis factor Mus musculus 77-86 9192827-10 1997 Neutralizing concentrations of anti-TNF-alpha antibody suppressed the Bryo plus IFN-gamma-induced NO2- production approximately by 50%, suggesting that NO2- produced by Bryo plus IFN-gamma-treated ANA-1 macrophages may involve both TNF-alpha-dependent and TNF-alpha-independent mechanisms. Nitrogen Dioxide 98-101 tumor necrosis factor Mus musculus 36-45 9192827-10 1997 Neutralizing concentrations of anti-TNF-alpha antibody suppressed the Bryo plus IFN-gamma-induced NO2- production approximately by 50%, suggesting that NO2- produced by Bryo plus IFN-gamma-treated ANA-1 macrophages may involve both TNF-alpha-dependent and TNF-alpha-independent mechanisms. Nitrogen Dioxide 152-155 tumor necrosis factor Mus musculus 36-45 9192827-10 1997 Neutralizing concentrations of anti-TNF-alpha antibody suppressed the Bryo plus IFN-gamma-induced NO2- production approximately by 50%, suggesting that NO2- produced by Bryo plus IFN-gamma-treated ANA-1 macrophages may involve both TNF-alpha-dependent and TNF-alpha-independent mechanisms. Nitrogen Dioxide 152-155 tumor necrosis factor Mus musculus 232-241 9192827-10 1997 Neutralizing concentrations of anti-TNF-alpha antibody suppressed the Bryo plus IFN-gamma-induced NO2- production approximately by 50%, suggesting that NO2- produced by Bryo plus IFN-gamma-treated ANA-1 macrophages may involve both TNF-alpha-dependent and TNF-alpha-independent mechanisms. Nitrogen Dioxide 152-155 tumor necrosis factor Mus musculus 232-241 7520469-4 1994 The inhibition of NO2- and NO3- release in mice injected with anti-tumor necrosis factor (TNF) and/or anti-interferon gamma (IFN-gamma) monoclonal antibody (mAb) before SEB challenge revealed that both cytokines were involved in SEB-induced NO overproduction. Nitrogen Dioxide 18-21 tumor necrosis factor Mus musculus 62-88 7953244-5 1994 The production of NO2- by TNF-alpha-, IFN-gamma- or IFN-gamma/TNF-alpha-treated macrophages from Toxoplasma-infected mice were significantly higher than that by resident macrophages, whereas lymphokine-treated group produced similar amount as that produced by resident macrophages. Nitrogen Dioxide 18-21 tumor necrosis factor Mus musculus 26-35 7953244-5 1994 The production of NO2- by TNF-alpha-, IFN-gamma- or IFN-gamma/TNF-alpha-treated macrophages from Toxoplasma-infected mice were significantly higher than that by resident macrophages, whereas lymphokine-treated group produced similar amount as that produced by resident macrophages. Nitrogen Dioxide 18-21 tumor necrosis factor Mus musculus 62-71 7514114-3 1994 When treated with the proinflammatory cytokines IFN-gamma, TNF-alpha, and IL-1 alpha, these fibroblast lines produce micromolar quantities of NO2- and NO3-, two stable end products of the NO pathway. Nitrogen Dioxide 142-145 tumor necrosis factor Mus musculus 59-68 8473748-6 1993 Neutralizing concentrations of anti-TNF mAb completely abrogated IFN-gamma- and IFN-gamma plus rTNF-alpha-induced NO2- production in ANA-1 macrophages, but only decreased by approximately 50% the synergistic interaction between IFN-gamma and picolinic acid. Nitrogen Dioxide 114-117 tumor necrosis factor Mus musculus 36-39 8473748-8 1993 Therefore, picolinic acid may affect NO2- production via both TNF-alpha-dependent and TNF-alpha-independent pathways. Nitrogen Dioxide 37-40 tumor necrosis factor Mus musculus 62-71 8473748-8 1993 Therefore, picolinic acid may affect NO2- production via both TNF-alpha-dependent and TNF-alpha-independent pathways. Nitrogen Dioxide 37-40 tumor necrosis factor Mus musculus 86-95 1452344-4 1992 Injection of neutralizing antibodies against TNF-alpha simultaneously with the rIFN-gamma completely inhibited both the release of NO2- by macrophages and their toxoplasmastatic activity. Nitrogen Dioxide 131-134 tumor necrosis factor Mus musculus 45-54 8423095-2 1993 Both NO2- production and inhibition of bacterial growth were suppressed by NG-monomethyl-L-arginine, a substrate inhibitor of nitrogen oxidation of L-arginine, and monoclonal antibodies (MAbs) to gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). Nitrogen Dioxide 5-8 tumor necrosis factor Mus musculus 229-256 8423095-2 1993 Both NO2- production and inhibition of bacterial growth were suppressed by NG-monomethyl-L-arginine, a substrate inhibitor of nitrogen oxidation of L-arginine, and monoclonal antibodies (MAbs) to gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). Nitrogen Dioxide 5-8 tumor necrosis factor Mus musculus 258-267 7681038-4 1993 Like M phi, these clones were found to release high levels of NO2- in response to recombinant interferon-gamma (rIFN-gamma) as a priming signal together with either bacterial lipopolysaccharide (LPS) or exogenous recombinant tumor necrosis factor-alpha (rTNF-alpha). Nitrogen Dioxide 62-65 tumor necrosis factor Mus musculus 225-252 2279740-6 1990 The level of NO2-, which is also a measurement of NO production, in the culture supernatant of TNF-alpha-activated macrophages can be progressively decreased to basal level with increasing concentrations of L-NMMA, but not with its D-enantiomer, D-NMMA. Nitrogen Dioxide 13-16 tumor necrosis factor Mus musculus 95-104 1898602-6 1991 However, TNF-alpha secretion was elevated in cultures undergoing phagocytosis and a relationship between hexosemonophosphate shunt activity and NO2- levels was evident. Nitrogen Dioxide 144-147 tumor necrosis factor Mus musculus 9-18 1431106-7 1992 Lastly, incubation of ANA-1 macrophages with anti-TNF mAb selectively inhibited the ability of IFN-gamma plus IL-2 to induce NO2- production and tumoricidal activity. Nitrogen Dioxide 125-128 tumor necrosis factor Mus musculus 50-53 1431106-8 1992 These results indicate that IFN-gamma plus IL-2-induced tumoricidal activity is dependent upon the metabolism of L-arginine to reactive nitrogen intermediates, and they establish a role for TNF-alpha as a required intermediate for IL-2-dependent NO2- production and tumoricidal activity. Nitrogen Dioxide 246-249 tumor necrosis factor Mus musculus 190-199 1729374-9 1992 Neutralizing antibodies against mouse TNF-alpha inhibited also the release of NO2- by rIFN-gamma-activated macrophages almost completely. Nitrogen Dioxide 78-81 tumor necrosis factor Mus musculus 38-47 1915557-4 1991 As shown here, the capacity of phagocytosis to elicit NO2- production by IFN-gamma-treated M phi was inhibited by antibody to murine recombinant tumor necrosis factor-alpha (rTNF-alpha), suggesting that phagocytosis enabled IFN-gamma to activate M phi via the induction of TNF-alpha as an autocrine second signal. Nitrogen Dioxide 54-57 tumor necrosis factor Mus musculus 145-172 1915557-4 1991 As shown here, the capacity of phagocytosis to elicit NO2- production by IFN-gamma-treated M phi was inhibited by antibody to murine recombinant tumor necrosis factor-alpha (rTNF-alpha), suggesting that phagocytosis enabled IFN-gamma to activate M phi via the induction of TNF-alpha as an autocrine second signal. Nitrogen Dioxide 54-57 tumor necrosis factor Mus musculus 175-184 1915557-5 1991 M phi NO2- production in response to rIFN-gamma and either exogenous TNF-alpha or Leishmania was strongly enhanced by prostaglandin E2, consistent with such a mechanism. Nitrogen Dioxide 6-9 tumor necrosis factor Mus musculus 69-78 1915557-9 1991 Phagocytosis also increased M phi NO2- production elicited by IFN-gamma plus TNF-alpha in L-arginine-deficient media. Nitrogen Dioxide 34-37 tumor necrosis factor Mus musculus 77-86 3142779-2 1988 Recombinant interferon-gamma (rIFN-gamma) and recombinant tumor necrosis factor (rTNF) synergize to induce nitrite (NO2-) and nitrate (NO3-) synthesis from L-arginine as well as to cause inhibition of the iron-dependent enzyme aconitase in macrophages. Nitrogen Dioxide 116-119 tumor necrosis factor Mus musculus 58-79