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GPI — TNF

Text-mined interactions from Literome

Vijaykumar et al., J Biol Chem 2001 (Inflammation) : These novel interactions are coupled to previously demonstrated PTK and PKC pathways, since the specific inhibitors of these kinases effectively blocked the GPI induced TNF-alpha production
Askari et al., Prostaglandins Other Lipid Mediat 2001 : We, therefore, examined the effects of TNF-alpha on Ang II-induced increases in PGI2 production in vascular smooth muscle cells ( VSMC )
Li et al., Acta Pharmacol Sin 2000 : The responses of antisense IRAK-2 ODN to IL-1 and TNF stimulated PGI2 release are different
Kalsi et al., Mol Cell Biochem 2002 : Therefore, we conclude that TNF-alpha through activation of endogenous PLC leads to cleavage of the GPI-linkage of E5'N resulting in loss of E5'N from the extracellular surface
Nitto et al., Br J Pharmacol 2002 : 2 TNF-alpha induced the release of GPI-80 from human neutrophils in a concentration- and time dependent manner ( in the range of 1-100 u ml(-1) and 30-120 min, respectively ), but did not affect surface GPI-80 levels ... 3 Cytochalasin B, genistein, and SB203580 but not PD98059 inhibited TNF-alpha stimulated GPI-80 release and neutrophil adherence at the same concentration ... In addition, TNF-alpha induced GPI-80 release was inhibited by blocking monoclonal antibodies specific to components of Mac-1 ( CD11b and CD18 ) ... 5 These findings indicate that TNF-alpha stimulated GPI-80 release from human neutrophils depends upon adherence via beta2 integrins
Itoh et al., Respirology 2003 : TNF-alpha and MIF also increased PGI2 production, but to a far lesser degree at high concentrations
Hazenbos et al., Blood 2004 (Inflammation) : Strikingly, after stimulation with IgG-ICs, tumor necrosis factor-alpha release, dendritic cell maturation, and antigen presentation were strongly reduced by GPI-anchor deficiency
Debierre-Grockiego et al., Infect Immun 2006 (Malaria, Falciparum) : Here we show that Pfj is able to down-regulate tumor necrosis factor alpha (TNF-alpha) production induced by the GPI of P. falciparum
Amaya et al., Pain 2009 (Disease Models, Animal...) : The PGI also induced a prominent increase in IL-1beta and TNF-alpha levels in the DRG and of cyclooxygenase-2 (COX-2) expression in neurons and satellite cells
Corradin et al., Eur J Immunol 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
Conroy et al., PloS one 2009 (Inflammation...) : Plasmodium falciparum GPI ( pfGPI ) enhanced C5a receptor expression ( CD88 ) on monocytes, and the co-incubation of monocytes with C5a and pfGPI resulted in the synergistic induction of cytokines ( IL-6, TNF , IL-1beta, and IL-10 ), chemokines ( IL-8, MCP-1, MIP1alpha, MIP1beta ) and the anti-angiogenic factor sFlt-1 in a time and dose dependent manner
Newman et al., J Immunol 1991 (Mycobacterium avium-intracellulare Infection) : The long term survival of peripheral blood derived human macrophages ( M phi ) from normal, healthy donors after infection with Mycobacterium avium intracellulare ( MAI ) correlates with the increased induction of TNF-alpha and IL-6 mRNA and protein by the infected M phi
Brenneis et al., J Biol Chem 2011 (Disease Models, Animal...) : Interestingly, we found that activation of E-prostanoid ( EP ) 2 and EP4 receptors, but not EP1, EP3, PGI(2) receptor ( IP ), thromboxane A(2) receptor ( TP ), PGD(2) receptor ( DP ), and PGF ( 2 ) receptor ( FP ), efficiently blocked LPS induced tumor necrosis factor a (TNFa) synthesis and COX-2 and mPGES-1 induction as well as prostaglandin synthesis in spinal cultures
Bogdan et al., Eur J Immunol 1990 : In the present study we investigated whether TNF-alpha activates M phi for killing of L. major parasites
Szabo et al., J Leukoc Biol 1990 : The difference in the M phi subset 's TNF response remained even after the FcRI- M phi subset received a 2.5-fold increase in stimulation with the classical M phi induction regimen of IFN gamma plus bacterial cell wall product
Watari et al., Int J Cancer 2012 : Low dose AMF-26 effectively inhibited the tumor necrosis factor-a (TNF-a)- or the interleukin-1ß (IL-1ß) induced production of ICAM-1 in human umbilical vascular endothelial cells ( HUVECs )
Laplante et al., J Biol Chem 2011 : In contrast, neither polymyxin B-treated nor delipidated ß ( 2 ) GPI stimulated TNF-a production
Xie et al., Mol Immunol 2013 (Antiphospholipid Syndrome) : Anti-ß ( 2 ) GPI/ß ( 2 ) GPI induced TF and TNF-a expression in monocytes involving both TLR4/MyD88 and TLR4/TRIF signaling pathways ... Overall, our results indicate that anti-ß ( 2 ) GPI/ß ( 2 ) GPI complex induced TF and TNF-a expression involving both TLR4/MyD88 and TLR4/TRIF signaling pathways and TLR4 and its adaptors might be molecular targets for therapy of antiphospholipid syndrome (APS)
Endo et al., Biochem Biophys Res Commun 1988 : Both IL-1 and TNF increased PGI2 production by EC in both a time- and dose dependent manner, and a combination of the two cytokines additively enhanced PGI2 production
Kawakami et al., Biochem Biophys Res Commun 1986 : The stimulation of PGI2 by cachectin/TNF is comparable to that observed with interleukin-1, the monokine previously suggested to be the principal mediator of this effect ... The ability of cachectin/TNF to stimulate PGI2 production suggests that it may play a role in producing depressed blood pressure or shock
Hauser et al., Arch Surg 1995 (Wounds and Injuries) : If so, TNF-alpha down-regulation might contribute to functional PM phi suppression after systemic injury
Douvdevani et al., J Am Soc Nephrol 1995 : It was found that clamping pHi to values below 6.5 led to a markedly reduced tumor necrosis factor-alpha production and phagocytosis
Orlinska et al., Immunopharmacology 1995 : In the presence of 100 microM phloretin or DIDS the pHi of activated monocyte was reduced to control value, TNF-alpha production was inhibited completely and total protein synthesis was inhibited by 61 % ... These data suggest that ( 1 ) TNF-alpha production, as other proteins, is dependent on the pHi of monocytes, and ( 2 ) TNF-alpha production, in contrast to total protein, is modulated by Na ( + ) -dependent HCO3-
Bradshaw et al., J Pharmacol Exp Ther 1995 : Activation of murine bone marrow derived macrophages ( BMDM phi ) with lipopolysaccharide (LPS) causes rapid expression of TNF-alpha , which as an autocrine factor enhances BMDM phi function through IL-1 beta and IL-6 production
Heise et al., J Virol 1995 (Cytomegalovirus Infections...) : We conclude that ( i ) M phi activation is a prominent part of inflammatory responses to herpesvirus infection and ( ii ) IFN gamma and TNF alpha play a critical role in both virus induced M phi activation and control of herpesvirus growth independent of T and B cells
Pruimboom et al., Prostaglandins Leukot Essent Fatty Acids 1994 : We conclude that LPS stimulation of hp-M phi from liver disease results in similar production of IL-1 beta, IL-6 and TNF-alpha , but that the profile of the eicosanoid production of these M phi stimulated with LPS and A23187 differs from M phi of other origin and species
Alleva et al., Immunobiology 1993 (Neoplasms, Experimental) : A PGE2-specific enzyme linked immunosorbent assay showed that TBH M phi T cell cultures contained significantly more PGE2 than those containing NH M phi , and that exogenous TNF-alpha increased PGE2 production in TBH M phi cultures more than in NH M phi cultures
Pomerantz et al., Biochemistry 1993 : Indeed, cholesterol enrichment attenuated IL-1 beta-, PDGF-, and TNF alpha induced PGI2 synthesis relative to controls and was consistent with the results of in vitro labeling experiments demonstrating that cholesterol enrichment reduced the incorporation of [ 35S ] methionine into immunoprecipitable COX-1 and COX-2 following induction by PDGF
Nwariaku et al., Shock 1995 (Shock, Hemorrhagic) : The purpose of this study was to determine if hemorrhagic shock alters the alveolar macrophage ( M phi ) tumor necrosis factor (TNF) response to lipopolysaccharide (LPS) stimulation
Schofield et al., J Immunol 1996 : The direct activation of endothelial cells by GPI does not require the participation of TNF or IL-1
Moore et al., J Immunol 1996 (Lupus Nephritis) : We hypothesized that TNF-alpha enhanced the M phi response to CSF-1 in MRL-lpr mice
Jungi et al., Immunol Lett 1996 : Here we show that human monocyte derived M phi respond to LPS by tumor necrosis factor-alpha release and procoagulant activity upregulation by a similar dose response curve in the presence or absence of serum, suggesting that humoral factors such as LBP are relatively unimportant in the activation of M phi
Sasaki et al., Blood 1997 (Hematologic Neoplasms...) : Phorbol 12-myristate 13-acetate ( PMA ), interleukin-1 (IL-1), IL-3, IL-6, granulocyte-macrophage colony stimulating factor ( GM-CSF ), thrombopoietin (TPO), and tumor necrosis factor-alpha (TNF-alpha) enhanced PGI2-R mRNA expression
Wen et al., Cell Biol Int 1997 : LPS, IL-1 beta and TNF alpha effectively enhanced BK-stimulated production of PGI2 by HPASMC, while IFN gamma had only a weak effect on BK-stimulated PGI2 production ... Bradykinin induced enhancement of PGI2 production by LPS, IL-1 beta and TNF alpha might be involved in the regulation of pulmonary vascular tension and prevent a paradoxical thrombogenic effect in endotoxin- or cytokine mediated inflammation and acute lung injury
Chou et al., J Neuroimmunol 1998 (Arthritis...) : Adrenergic regulation of LPS stimulated TNF production by M phi isolated from rats with streptococcal-cell-wall ( SCW ) -induced arthritis has been examined