◀ Back to IRF6

GPI — IRF6

Text-mined interactions from Literome

Tang et al., Immunology 1999 : The LPS induced NO and PGI2 production from these cells was increased significantly by rCGRP at 0.01-10 nm in a concentration dependent manner, which was blocked by L-NMMA and indomethacin
Janowiak et al., Prostaglandins Other Lipid Mediat 1999 : Studies were conducted to determine the effects of reproductive phase and lipopolysaccharide (LPS) on production of PGI2 and amounts of cyclooxygenase protein in uterine, mammary, mesenteric, and renal arteries
Arbabi et al., Surgery 2000 : Here, we hypothesized that HTS and LPS may induce PGI ( 2 ) production by increasing cyclooxygenase (COX) expression
Shaw et al., J Immunol 1979 (Leukemia, Experimental) : Indomethacin induced blockade of the M phi cyclooxygenase pathway inhibited PG synthesis by LPS stimulated , primed M phi without affecting the return of cytolytic activity
Punchard et al., Mediators Inflamm 2000 (Colitis, Ulcerative) : LPS stimulated both PGE2 and PGI2 by PBMNC from HS and UC patients
Haskó et al., Immunology 2001 : In the present study, we investigated the effect of sulphasalazine and two related compounds - sulphapyridine and 5-aminosalicylic acid - on M phi activation induced by bacterial lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma)
Meng et al., J Surg Res 2001 (Anoxia) : Inhibition of PDE may be a therapeutic approach for suppression of synergistic induction of M phi TNF-alpha production by hypoxia and LPS in posttraumatic tissue
Luo et al., Hunan Yi Ke Da Xue Xue Bao 2000 : In vitro experiment, we found that AG and PDTC inhibited the apoptosis of M phi induced by IFN ( 100 U.ml-1 ) + LPS ( 10 micrograms.ml-1 ) by using DNA gel electrophoresis analysis ... These evidences support that NO and active oxygen species may be involved in the apoptosis process of peritoneal M phi induced by LPS in mice
Martin et al., J Clin Invest 1992 (Respiratory Distress Syndrome, Adult) : Neither LPS nor LPS and LBP affected pHi or [ Cai++ ] in alveolar macrophages
Prajgrod et al., Agents Actions 1992 : While Dex was without effect, IL-1 and LPS stimulated PGI2 in a concentration- and time dependent manner
Chien et al., Chin J Physiol 2004 : Our results indicated that ( 1 ) LPS stimulated pHi elevation was PKC dependent ; ( 2 ) After 30 min stimulation, LPS increased PLD activity via a measured production of 3H-phosphatidylethanol from phosphatidic acid and the initiation of PLD1a mRNA expression started ; ( 2 ) LPS stimulated IL-2 R expression but not IL-2 and IL-4 secretion
Guo et al., Zhonghua Shao Shang Za Zhi 2005 : MP could obviously inhibit the expression of TLR4, TNF-alpha and IL-6 mRNA in LPS stimulated murine PM phi
Danon et al., Agents Actions 1991 : On the other hand, LPS stimulated PGI2 production in adrenalectomized rats, although the latter had reduced capacity to synthesize PGI2, compared with sham operated rats
Wang et al., Proc Natl Acad Sci U S A 2006 (Atherosclerosis) : Stimulation of mPGES-1 ( -/- ) VSMC and macrophages with bacterial LPS increased PGI ( 2 ) and thromboxane A ( 2 ) to varied extents
Nestel et al., J Exp Med 1992 (Disease Models, Animal...) : The data provide evidence that during GVHD M phi are primed as a result of the allogeneic reaction and that endogenous LPS therefore triggers M phi production of TNF-alpha resulting in the symptoms characteristic of acute GVHD
Stout et al., Cell Immunol 1992 : Activation of the M phi-c by LPS + rIFN-gamma could be completely blocked by anti-TNF-alpha antibodies
Tan et al., J Immunol 2007 : In addition to the direct effect, histamine was found to amplify LPS stimulated COX-2 expression and PGE ( 2 ) and PGI ( 2 ) production
Corradin et al., Eur J Immunol 1991 : Furthermore, anti-TNF antibody failed to inhibit M phi responses to rIFN-gamma and bacterial lipopolysaccharide (LPS) in the presence or absence of Leishmania ; also exogenous rTNF-alpha did not significantly affect NO2- production by IFN-gamma/LPS cultures despite a strong enhancement by Leishmania
Yoshimura et al., Nihon Geka Gakkai Zasshi 1990 : High levels of gamma-IFN mRNA in PHA stimulated PBL or IL-1 (beta) mRNA in LPS stimulated m phi were present in normal individuals, but not in CsA treated recipients as judged by hybridization to a cloned human gamma-IFN or IL-1 (beta) cDNA probe
von Kleist et al., Immunobiology 1990 : LPS , IL6, and IL4 caused induction of up to 15 % Fo+ and Ia+ M phi after a 4 d culture period
Laplante et al., J Biol Chem 2011 : Here, we show that both LPS and TLR4 are required for ß ( 2 ) GPI to bind to and activate macrophages
Stout et al., J Immunol 1989 : IFN-gamma, in the absence of LPS, could activate the elicited M phi and to a lesser and more variable degree, the resident M phi Only the M phi-c consistently required both IFN-gamma and LPS for induction of cytostatic activity
Zhang et al., Transplantation 1989 : In contrast, LPS increases PGE2 and PGI2 synthesis and alters their relative concentrations, diminishes the relative concentration of free arachidonic acid, and enhances the formation of new metabolites that are products of cyclooxygenase activity
Yoshimura et al., J Clin Immunol 1989 : High levels of gamma-IFN mRNA in phytohemagglutinin ( PHA ) -stimulated PBMC or IL-1(beta) mRNA in lipopolysaccharide (LPS) stimulated m phi were present in normal individuals but not in CsA treated recipients as judged by hybridization to a cloned human gamma-IFN or IL-1(beta) cDNA probe
Lucchiari et al., Immunobiology 1989 (Hepatitis, Viral, Animal) : Using specific antibodies, we have shown that the delayed MHV3 replication in LPS activated A/J M phi was due, in part, to IFN-alpha/beta
Morris et al., Cornell Vet 1989 : The only significant difference in the in vitro LPS induced production of TxA2 and PGI2 by peritoneal macrophages between immunized and control horses was a greater production of TxA2 by macrophages from immunized horses in response to 10 ng/ml LPS ( p less than 0.05 )
Pohlman et al., J Surg Res 1988 : At 10 ( -5 ) M, both LPS and lipid A produced significant BEC cytotoxicity ( percentage cytotoxicity 69 +/- 4 for LPS and 51 +/- 11 for lipid A ) and induced a variable but consistent increase in the release of PGI2 ( 11- to 73-fold increase for LPS and 4- to 6-fold increase for lipid A )
Gifford et al., Int J Cancer 1986 (Neoplasms, Experimental) : Optimal A9 killing and CF secretion, equivalent to the killing of about 1000 AcD pretreated A9 cells by a single macrophage, were obtained following activation of JBM phi by LPS
Ulevitch et al., Fed Proc 1984 : The potential role of the M phi in regulating the binding of LPS to high-density lipoproteins through the induction of acute phase proteins is also considered
Schlager et al., Cell Immunol 1983 (Neoplasms, Experimental) : LK was shown to be able to prime and trigger whereas LPS could only trigger LK-primed M phi for tumor cytotoxicity
Theus et al., Toxicol Appl Pharmacol 1993 : Although control animals showed a typical pattern of requiring both interferon (IFN)-gamma and lipopolysaccharide (LPS) for m phi activation, m phi from propanil treated animals were cytotoxic when induced with LPS alone
Bidani et al., J Leukoc Biol 1995 : The results demonstrate that V-ATPase activity is an important determinant of the effector functions of LPS activated m phi
Turek et al., J Leukoc Biol 1994 : Lipopolysaccharide (LPS) stimulated LC and MC m phi s produced more TNF than m phi s from pigs fed CO, LO, and MO diets
West et al., J Trauma 1994 : LPS1 markedly inhibited M phi TNF release by LPS2, but hypoxia had no effect on LPS2 triggered TNF release
Watanabe et al., Prostaglandins Leukot Essent Fatty Acids 1993 : We investigated the potency of various serotypes of lipopolysaccharides (LPS) by examining LPS induced stimulation of PGI2 production and suppression of ACE activity in cultured human umbilical vein endothelial cells ( HUVEC )
Ensor et al., Am J Physiol 1994 (Fever) : In LPS stimulated HuMoM phi incubated at 40 degrees C, TNF-alpha release was almost completely inhibited ( 76 +/- 76 pg TNF-alpha/10 ( 6 ) cells ; P < 0.01 compared with LPS stimulated HuMoM phi at 37 degrees C ), but release of IL-6 was preserved ( 1,600 +/- 780 pg IL-6/10 ( 6 ) cells ) ... Our results show that IL-6 expression persisted at incubation temperatures in the upper end of the physiological range that induced heat shock and attenuated the expression of functionally active TNF-alpha in LPS stimulated HuMoM phi
Watanabe et al., Prostaglandins Leukot Essent Fatty Acids 1993 : Although the concentrations or IL-1 beta and TNF alpha in the post-culture medium of HUVEC treated with LPS-Mo-CM were much higher than those with Mo-CM, LPS-Mo-CM which was made with 13,000/ml of mononuclear cells and 1 microgram/ml of LPS did not significantly augment the subsequent PGI2 production by HUVEC as compared with Mo-CM made with the same numbers of mononuclear cells
Adams et al., Infect Immun 1993 : LAMH37Ra and LPS could induce the production of NO2- in both normal and IFN-gamma primed M phi, whereas LAM ( Erdman ) could stimulate NO2- production only in primed M phi
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
Kirikae et al., Biochem Biophys Res Commun 1996 : These data also suggest that the binding of taxoid/LPS to tubulin is not essential for the M phi activation
Jungi et al., Immunol Lett 1996 : Both serum dependent and serum independent activation of M phi by LPS require cellular CD14, as evidence by blocking studies with CD14-specific antibodies
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