Gene interactions and pathways from curated databases and text-mining

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LBP — TNF

Text-mined interactions from Literome

Hermann et al., Eur J Immunol 2002 : LBP enhanced TNF-alpha release of human peripheral blood mononuclear cells ( PBMC ) upon LPS but not LTA stimulation
Nakatani et al., Alcohol Clin Exp Res 2002 (Liver Diseases, Alcoholic) : To determine the pathophysiological roles of macrophages in alcoholic liver disease, we examined the effect of ethanol on TNF-alpha secretion of rat Kupffer cells, alveolar macrophages, and peritoneal macrophages in the presence or absence of LBP ... Serum LBP enhances the secretion of TNF-alpha by macrophages
Tada et al., Microbiol Immunol 2002 : The TNF-alpha production triggered by reference LPS and purified fungal mannans required the presence of LPS binding protein (LBP) , and these responses were inhibited by anti-CD14 and anti-TLR4 antibodies, but not by anti-TLR2 antibody
Martin et al., J Clin Invest 1992 (Respiratory Distress Syndrome, Adult) : Thus, immunoreactive LBP accumulates in lung lavage fluids in patients with lung injury and enhances LPS stimulated TNF alpha gene expression in alveolar macrophages by a pathway that depends on the CD14 receptor
Weber et al., Immunity 2003 (Pneumococcal Infections) : LBP enhanced PCW induced cell signaling and TNF-alpha release
Kitazawa et al., Alcohol Clin Exp Res 2003 (Alcoholic Intoxication) : The production of TNF-alpha by these cells incubated with endotoxin 100 ng/ml in the presence or absence of LBP ( 1 % rat serum ) was determined
Li et al., Chin J Traumatol 2003 : The level of plasma endotoxin peaked at 1 h after LPS injection, then declined, but was still higher than that of the normal group at 12 h ; intrahepatic expression of LBP mRNA and plasma LBP increased with time after LPS stimulation ; TNF-alpha and IL-6 in plasma increased with upregulation of LBP expression ; there were significant differences between the normal group and endotoxemia groups ( P < 0.05 )
Fang et al., Burns Incl Therm Inj 2004 (Burns) : This study investigates whether tumor necrosis factor ( TNF-alpha ) might be responsible for the LBP formation during endogenous endotoxemia postburn
Mathison et al., J Immunol 1992 : To define the role of LBP in regulating responses to LPS we have examined TNF release in rabbit peritoneal exudate macrophages ( M phi ) stimulated with LPS or with complete or partial lipid A preparations in the presence or absence of LBP ... However, consistent with our previous observations that these structures bind to LBP, TNF production was increased in the presence of LBP ... In contrast, LBP did not enhance or inhibit TNF production produced by heat killed Staphylococcus aureus, peptidoglycan isolated from S. aureus cell walls, or PMA
Chen et al., Phytother Res 2009 : In vitro studies showed that LBP and LBPF1-5 activated transcription factors NF-kappaB and AP-1 by RAW264.7 macrophage cells, induced TNF-alpha , IL-1beta, IL-12p40 mRNA expression, and enhanced TNF-alpha production in a dose dependent manner
Grube et al., J Biol Chem 1994 (Carcinoma, Hepatocellular...) : To examine this phenomenon in more detail, we evaluated the capacity of IL-6, IL-1, and tumor necrosis factor to induce LBP synthesis in HepG2 cells in the presence or absence of dexamethasone
Gallay et al., Proc Natl Acad Sci U S A 1994 (Shock, Septic) : This demonstrated that anti-LBP IgG could block the LBP mediated TNF release upon LPS challenge
Jahr et al., Scand J Immunol 1995 : In this study we examined the involvement of human serum, recombinant lipopolysaccharide binding protein ( rLBP ), recombinant ( r ) CD14, CD14 antibodies and recombinant bactericidal permeability increasing factor ( rBPI ) in the induction of TNF by Salmonella minnesota LPS of different polysaccharide chain lengths
Wan et al., Infect Immun 1995 : In contrast to IL-6 and LPS, in the presence of 10 ( -6 ) M dexamethasone, IL-1 and tumor necrosis factor (TNF) led to maximal LBP mRNA induction levels, 4.7- and 3.8-fold, respectively, suggesting that IL-6 and LPS stimulate LBP expression by mechanisms different from those of IL-1 and TNF
Jahr et al., Infect Immun 1997 : In this study we have investigated the effects of soluble CD14 ( sCD14 ), lipopolysaccharide binding protein (LBP), and bactericidal/permeability increasing factor ( BPI ) on poly ( M ) binding to monocytes and induction of TNF production ... We show that LBP increased the TNF production from monocytes stimulated with poly ( M ) ... BPI was found to inhibit TNF production from monocytes stimulated with poly ( M ) in the presence of LBP , LBP-sCD14, or 10 % human serum ... Our data demonstrate a role for LBP , LBP-sCD14, and BPI in modulating TNF responses of defined polysaccharides
Amura et al., J Immunol 1997 : We have investigated the effects of human LPS binding protein (LBP) and human bactericidal/permeability increasing protein ( BPI ) on LPS dependent activation of mouse thioglycolate elicited peritoneal macrophages in vitro, in comparison with human PBMCs. Confirming earlier published studies, BPI inhibited, and LBP enhanced , the ability of LPS to stimulate PBMC production of the cytokines TNF-alpha and IL-6