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IL8 — TLR4

Text-mined interactions from Literome

Yang et al., J Biol Chem 2000 : TLR4 mediated NF-kappaB reporter activity and IL-8 production was enhanced by the expression of MD-2 ... This study demonstrates that expression of both TLR4 and MD-2 is required for LPS to activate or augment the MAP kinase pathways, Elk-1 stimulation, and IL-8 generation
Mita et al., Br J Haematol 2001 : TLR4 surface expression paralleled LPS induced phagocytosis and TLR4 neutralizing antibody partially inhibited LPS induced IL-8 production in HL-60 derived monocytic cells, but not in HL-60 derived granulocytic cells
Dziarski et al., J Endotoxin Res 2000 : Therefore, TLR2 is a functional receptor for both Gram positive and Gram negative bacteria and it induces activation of IL-8
Liang et al., Sheng Wu Yi Xue Gong Cheng Xue Za Zhi 2002 : [ Assessment of the role of TLR-4 in shear-stress induced IL-8 gene transcription activation in vascular endothelial cells by gene mutation and gene transfection technology ] ... This study is to evaluate the role of TLR-4 in lower laminar shear stress induced interleukin-8 gene transcription activation in vascular endothelial cells by using gene mutation and transfection techniques
O'Reilly et al., Biochem Biophys Res Commun 2003 : Full length A20 inhibited the ability of TLR-4 to activate the transcription factors, NF-kappa B and AP-1, and induce the chemokine IL-8
Sabroe et al., J Immunol 2003 : Activation of either TLR2 or TLR4 caused changes in adhesion molecule expression, respiratory burst ( alone, and synergistically with fMLP ), and IL-8 generation, which was, in part, dependent upon p38 mitogen activated protein kinase signaling
Pivarcsi et al., Int Immunol 2003 : The microbial compound induced increase in IL-8 gene expression could be inhibited by anti-TLR2 and anti-TLR4 neutralizing antibodies, suggesting that TLRs are involved in the pathogen induced expression of this pro-inflammatory cytokine
Devaney et al., FEBS Lett 2003 (Cystic Fibrosis) : We demonstrate that human embryonic kidney (HEK)293 cells transfected with a TLR4 cDNA ( HEK-TLR4 ) express TLR4 mRNA and protein and induce IL-8 promoter activity in response to NE. Treatment of both HEK-TLR4 and human bronchial epithelial cells with NE decreases TLR4 protein expression
Tamandl et al., Shock 2003 (Inflammation...) : Here, we evaluated TLR-4 expression of isolated monocytes in the presence of tumor necrosis factor (TNF)-alpha, interleukin (IL) 6, IL-8 , and IL-10, and we investigated cellular activation of this treatment
Ryan et al., Infect Immun 2004 : Reactive oxygen and nitrogen species differentially regulate Toll-like receptor 4-mediated activation of NF-kappa B and interleukin-8 expression
Becker et al., Toxicol Appl Pharmacol 2005 : When NHBE were stimulated with PM ( 2.5-10 ), PM2.5, and UF PM, in the presence or absence of inhibitors of TLR2 and TLR4 activation, a blocking antibody to TLR2 inhibited production of IL-8 , while TLR4 antagonist E5531 or the LPS inhibitor Polymixin B had no effect
Köllisch et al., Immunology 2005 : The TLR ligands peptidoglycan, Pam3Cys and flagellin which bind to TLR2, TLR1/TLR2 heterodimer, and TLR5, respectively, also induced IL-8 secretion, whereas no IL-8 was induced by LPS, R-848, loxoribine and cytosine guanine dinucleotide containing oligodeoxynucleotide
Raffatellu et al., Infect Immun 2005 : Collectively, these data suggest that the scarcity of neutrophils in intestinal infiltrates of typhoid fever patients is due to a capsule mediated reduction of TLR dependent IL-8 production in the intestinal mucosa
Maldonado-Bernal et al., Parasite Immunol 2005 : The interaction of LPPG with TLR2 and TLR4 resulted in activation of NF-kappaB and release of interleukin (IL)-10, IL-12p40, tumour necrosis factor (TNF)-alpha, and IL-8 from human monocytes
Kramer et al., J Leukoc Biol 2006 (Crohn Disease) : Moreover, they lack MDP induced enhancement of TLR mediated tumor necrosis factor alpha, interleukin (IL)-12 , and IL-10 production, which is observed in control DC with intact NOD2
Baruah et al., J Leukoc Biol 2006 : C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells ; PTX3 inhibits both events
Karimi et al., Respir Res 2006 : Then, Toll-like receptor neutralization was performed to study the involvement of Toll-like receptor-4 in IL-8 production ... The IL-8 production is dependent on Toll-like receptor 4 stimulation and LPS is not involved
El-Obeid et al., Biochem Biophys Res Commun 2006 : Effect of herbal melanin on IL-8 : a possible role of Toll-like receptor 4 (TLR4)
Mueller et al., J Immunol 2006 : TLR4/MD-2 mediated LPS uptake and TLR ligand induced I-kappaBalpha phosphorylation and IL-8 secretion were significantly diminished in Th2 cytokine primed IECs
Erridge et al., Atherosclerosis 2007 (Atherosclerosis) : OxPAPC induction of IL-8 was not blocked by the TLR4 specific antagonist Rhodobacter sphaeroides LPS in human aortic endothelial cells, though OxPAPC potently inhibited TLR4 mediated IL-8 induction in these cells ... TLR4 signalling does not contribute to OxPAPC induced IL-8 expression in human epithelial HEK-293, monocytic THP-1 or aortic endothelial cells
Broad et al., Immunology 2007 : In this study we have shown that, whilst NF-kappaB activation and production of TNF-alpha and interleukin-12 by murine RAW264.7 and J774.2 cells in response to stimulation by TLR4, -5, -7 or -9, was reduced by prior stimulation with TLR4 , -5, -7 or -9 ligands, the primary stimulation of TLR3, which does not use the MyD88 pathway, did not reduce the TNF-alpha or interleukin-12 responses to subsequent TLR stimulation
Gao et al., Zhonghua Yan Ke Za Zhi 2006 : The activity of IkappaBalpha in THCE cells was decreased to 10.31 +/- 1.30 ( gray scale value ) and 8.15 +/- 2.37 at 30 min after challenged with AF mycelium or supernatant extract agent compared to 51.57 +/- 5.58 and 49.23 +/- 3.49 of control group ( P < 0.01 ), and was reverted at 2 h. The secretion of IL-8 and TNF-alpha was partly inhibited by blocking TLR2 or TLR4 ( P < 0.05 ), obviously inhibited by blocking TLR2 and TLR4 ( 50 % and 40 % compared to that of control group ) ( P < 0.01 ) when challenged with AF mycelium. And that was markedly inhibited by blocking TLR4 or blocking TLR2 and TLR4 when challenged with AF supernatant ( P < 0.01 ). The secretion of IL-8 and TNF-alpha was not inhibited by blocking TLR2 when challenged with AF supernatant ( P > 0.05 )
Berndt et al., Am J Physiol Lung Cell Mol Physiol 2007 (Airway Obstruction...) : Elevated TLR4 expression and lack of A20 upregulation in bronchial epithelial cells from RAO affected horses may contribute to elevated IL-8 production, leading to exaggerated neutrophilic airway inflammation in response to inhalation of stable dust
Cho et al., Immunol Lett 2007 (Arthritis, Rheumatoid) : Thus, TLR-2 activation in RA FLS by microbial constituents could be involved in the induction of VEGF and IL-8 and thereby promote inflammation either directly or via angiogenesis
Wrann et al., J Immunol 2007 (Sepsis) : In addition, PI3K inhibition resulted in strongly elevated TLR-4 mediated generation of IL-1beta and IL-8 in neutrophils when these cells were co-stimulated with C5a
Uehara et al., Mol Immunol 2007 : Anti-RP3 Abs markedly promoted the release of IL-8 induced by chemically synthesized TLR and NOD ligands mimicking bacterial components : TLR2-agonistic lipopeptide ( FSL-1 ), TLR3-agonistic poly I:C, TLR4-agonistic lipid A ( LA-15-PP ), TLR7/8-agonistic single stranded RNA ( ssPolyU ), TLR9-agonistic bacterial CpG DNA, NOD1-agonistic FK156/565 and NOD2-agonistic muramyldipeptide ( MDP ) in THP-1 cells and human peripheral blood mononuclear cells, although sole incubation with anti-PR3 Abs induced only a low level of IL-8
Kanczkowski et al., Horm Metab Res 2007 (Adrenal Cortex Neoplasms) : The aim of this study was to clarify the role of different TLR ligands in IL8 production in NCI-H295R cells
Yokota et al., FEMS Immunol Med Microbiol 2007 (Inflammation) : Weak IL-8 induction by H. pylori LPS preparations was suppressed by expression of a dominant negative mutant of TLR2 but not of TLR4
Sawa et al., J Histochem Cytochem 2008 : The LPS induced IL-6, IL-8 , VCAM-1, and ICAM-1 production in LEC was suppressed by the introduction of TLR4-specific small interfering RNA, and also by anti-TLR4 , nobiletin, and CAPE pretreatment
Koff et al., Am J Physiol Lung Cell Mol Physiol 2008 : We conclude that multiple TLR ligands induce airway epithelial cell production of IL-8 and VEGF via a Duox1 -- > ROS -- > TACE -- > TGF-alpha -- > EGFR phosphorylation pathway
Buchholz et al., Infect Immun 2008 (Inflammation) : IL-8 induced at 30 h postinfection by C. trachomatis was dependent on NOD1 signaling through RIP2 ; however, the IL-8 response was independent of MyD88 dependent TLR signaling
Wang et al., Blood 2008 : We and others have reported that Toll-like receptor ( TLR ) proteins are present on human neutrophils and that granulocyte-macrophage colony stimulating factor ( GM-CSF ) treatment enhances IL-8 ( CXCL8 ) secretion in response to stimulation with TLR ligands
Heo et al., Immunol Lett 2008 (Inflammation) : Moreover, NOS inhibitor ( L-NAME ) and anti-TLR 4mAb reduced the LPS induced NO, IL-8 and VEGF production and ICAM-1 expression
Kuo et al., J Am Soc Nephrol 2008 (Ischemia...) : Furthermore, experiments with toll-like receptor 4 (TLR-4)-and TLR-2-deficient mice demonstrated that uric acid induced exocytosis of Weibel-Palade bodies is mediated by TLR-4 and that uric acid induced release of IL-8 requires both TLR-2 and TLR-4
Abdollahi-Roodsaz et al., Arthritis Rheum 2008 (Arthritis, Infectious...) : Shift from toll-like receptor 2 (TLR-2) toward TLR-4 dependency in the erosive stage of chronic streptococcal cell wall arthritis coincident with TLR-4 mediated interleukin-17 production
Bhattacharyya et al., Inflamm Bowel Dis 2009 : DSS induced increases in phospho-IkappaBalpha, nuclear NFkappaB ( p65 ), and IL-8 secretion in human colonic epithelial cells in tissue culture are attributable to a reactive oxygen species ( ROS ) -induced pathway of inflammation, and do not require TLR4 , MyD88, or Bcl10, which are associated with the innate immune pathway of NFkappaB-IL-8 activation
Berndt et al., Equine Vet J 2009 (Airway Obstruction...) : In human airway epithelium, TLR2 activation leads to interleukin (IL)-8 production
Hammad et al., Nat Med 2009 (Asthma...) : TLR4 triggering on structural cells caused production of the innate proallergic cytokines thymic stromal lymphopoietin, granulocyte-macrophage colony stimulating factor, interleukin-25 and interleukin-33
Abate et al., J Lipid Res 2010 (Inflammation) : Surfactant lipids regulate LPS induced interleukin-8 production in A549 lung epithelial cells by inhibiting translocation of TLR4 into lipid raft domains
Marsh et al., J Neurosci 2009 (Infarction, Middle Cerebral Artery...) : TLR4 can induce both IFNbeta and interferon stimulated genes through its adapter molecule Toll/interleukin receptor domain containing adaptor inducing IFNbeta ( TRIF ) and the IRF3 transcription factor
Choi et al., Atherosclerosis 2010 : This study suggests that GSA induces expression of IL-8 in VSMCs and that TLR-4 , mitogen activated protein kinases, NF-kappaB, and NADPH oxidase are involved in that process
Lee et al., J Parasitol 2010 : We also performed reverse transcriptase-polymerase chain reaction ( RT-PCR ) and flow cytometry to determine whether TLR and MUC expression is regulated by interferon (IFN)-gamma, interleukin-4 , or monoclonal antibodies ( mAbs ) against G. seoi 46 kDa antigen
Im et al., Mol Immunol 2009 : Collectively, these results suggest that flagellin induced IL-8 expression requires formation of lipid rafts, intracellular TLR activation, and subsequent activation of PKC and MAP kinases leading to the activation of the transcription factors NF-kappaB and NF-IL6 in human alveolar type II epithelial cells
Cheng et al., Infect Immun 2010 : Although protease activated receptor 1 (PAR1) and PAR2 ligation can moderately upregulate Toll-like receptor 4 (TLR4) mediated IL-8 production, no effect on the C. albicans induced cytokine was apparent
Suzuki et al., J Dent Res 2009 (Gingival Overgrowth) : In human gingival fibroblasts, cyclosporin alone did not induce evident inflammatory responses, but augmented the expression of CD54 and the production of interleukin (IL)-6 and IL-8 induced by TLR ligands, whereas phenytoin attenuated those responses
Manuse et al., Virology 2010 : Unexpectedly, TLR3 activation in infected cells led to enhanced IL-8 secretion, which correlated with increased RIG-I expression
Khan et al., J Immunol 2010 : Conversely, stable overexpression of Sigirr diminished NF-kappaB mediated IL-8 responses to TLR ligands
Greene et al., Mediators Inflamm 2010 (Cystic Fibrosis) : Here we investigate the inhibitory capacity of nicotine against TLR2- and TLR4 induced IL-8 production by CFTE29o- airway epithelial cells, determine the role of alpha7-nAChR ( nicotinic acetylcholine receptor ) in these events, and provide data to support the potential use of safe nicotine analogues as anti-inflammatories for CF
Hutchinson et al., Neuroscience 2010 : Live imaging of TLR4 activation in RAW264.7 cells and TLR4 dependent interleukin-1 release from BV-2 microglia revealed that amitriptyline blocked TLR4 signaling
Li et al., Wei Sheng Wu Xue Bao 2010 (Streptococcal Infections) : The cell wall of Streptococcus mutans upregulated the expression of TLR4 and induced the production of inflammatory cytokines IL-6 and IL-8 , indicating that the expression of TLR4 of EAhy926 cells may elicit a TLR4 mediated innate immune response and contribute to production of inflammatory cytokines IL-6 and IL-8
Han et al., Vet Microbiol 2010 : Involvement of TLR21 in baculovirus induced interleukin-12 gene expression in avian macrophage-like cell line HD11
Piazza et al., Innate Immun 2011 : High concentrations of hemin ( 50 µM ) triggered TLR4 mediated IL-8 production in the human HEK293/TLR4 cell line in the absence of the co-receptors CD14 and MD-2 ; the latter an essential co-receptor for TLR4 activation by endotoxin
He et al., J Cell Biochem 2010 : The activation of TLR4 by LPS modulated the expression of TLRs, induced the phosphorylation of NF-kappaB, P38, and ERK42/44, and up-regulated the gene expression of cytokines IL-8 , IFN-alpha, IFN-beta, and TNF-alpha, suggesting EPCs expressed functional TLR4
Säve et al., Infect Immun 2010 : The present study suggests that enhanced ATP release and P2Y receptor activation during urinary tract infection may represent a novel, non-TLR4 mediated mechanism for production of proinflammatory IL-8 in human urinary tract epithelial cells
Yin et al., Biochem Biophys Res Commun 2010 (Urinary Tract Infections) : TLR4 promotes secretion of IL-6 and IL-8 , mediates inhibition of bladder epithelial cell ( BEC ) bacterial invasion, and mediates expulsion of uropathogenic Escherichia coli from BECs
Piconi et al., AIDS 2010 (HIV Infections) : Activated T cells ( Ki67 ( + ) ), Treg lymphocytes ( CD4 ( + ) /CD25high/Foxp3+ ), divided into naive and activated cells based on PD1 expression, interleukin (IL)-10 and transforming growth factor ( TGF ) -beta production, annexin V, activation of caspases 8 and 9, Toll-like receptor (TLR)2 and TLR4 expression on immune cells, and plasma lipopolysaccharide (LPS) concentration were analyzed
Chung et al., J Infect Dis 2010 (Hepatitis C, Chronic) : Alloantigen presentation by monocytes isolated from HCV infected patients results in impaired production of interleukin 17 by naive CD4 ( + ) T cells in the presence of TLR ligands
Li et al., Cardiovascular diabetology 2010 : Stimulation of TLR2 or TLR4 induced NF-?B activation, and the expression of ICAM-1, IL-6 and IL-8
Li et al., Int J Mol Med 2011 : In addition, Atg7 gene expression silencingled to down-regulation of TLR mediated IL-8 expression in IECs, which indicates a potential role of autophagy in generating innate-immune responses
John et al., Exp Lung Res 2011 (Cystic Fibrosis) : Nevertheless, cystic fibrosis ( CF ) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF. The authors have shown that in CF bronchial epithelial cells, a reduced surface expression of TLR-4 causes a diminished interleukin (IL)-8 and IL-6 response upon lipopolysaccharide (LPS) stimulation
Okogbule-Wonodi et al., Dig Liver Dis 2012 : Toll-like receptor 4 expression was constitutive and Toll-like receptor 4 receptor blockade reduced IL-8 production by 42 % ( P=0.0262 )
Lee et al., J Agric Food Chem 2012 : The endothelial up-regulation of IL-8 secretion by resistin entailed toll-like receptor 4 (TLR4) activation, but caffeic acid diminished IL-8 production and TLR4 induction
Hanamsagar et al., Trends Immunol 2012 : TLR signaling triggers the transcriptional activation of pro-interleukin-1ß ( pro-IL-1ß ) and pro-IL-18 that are processed into their active forms by the inflammasome
Xia et al., J Pineal Res 2012 (Inflammation) : As expected, melatonin inhibited TLR4 mediated tumor necrosis factor alpha ( TNF-a ), interleukin (IL)-1ß , IL-6, IL-8, and IL-10 in LPS stimulated macrophages
Wang et al., Zhongguo Zhong Xi Yi Jie He Za Zhi 2012 : LPS induced platelet activation by TLR4 and released sCD40L and beta-TG, while the release of platelet IL-8 was not dependent on platelet TLR4-LPS pathway
Villacres et al., J Infect Dis 2012 (HIV Infections...) : Peripheral blood mononuclear cells ( PBMCs ) obtained at baseline were used to measure interleukin 1ß (IL-1ß), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 12 (IL-12), and tumor necrosis factor a (TNF-a) responses to Toll-like receptor (TLR) 3 and TLR4 stimulation
He et al., Int Endod J 2013 : Whether TLR4/MyD88/NF-?B was involved in the LPS induced up-regulation of IL-8 in hDPSCs was determined using transient transfection, luciferase assay and ELISA
Fu et al., Int Immunopharmacol 2012 : Furthermore, geniposide inhibited the expression of TLR4 in LPS stimulated primary mouse macrophages and inhibited the LPS induced IL-8 production in HEK293-mTLR4/MD-2 cells
Ding et al., Gene 2012 (Myocardial Reperfusion Injury) : The results demonstrated that fewer neutrophils infiltrated in the myocardium of TLR4-mutant mice after myocardial I/R and that TLR4 deficiency markedly decreased the ischemic injury caused by ischemia/reperfusion, and inhibited the expression of HMGB1, TNF-a, and IL-8 , all of which were up-regulated by ischemia/reperfusion
Li et al., eLife 2012 : A sequence containing 13 nucleotides near the active site of 23S rRNA ribozyme, which catalyzes peptide bond synthesis, was both necessary and sufficient to trigger TLR13 dependent interleukin-1ß production
Koblansky et al., Immunity 2013 (Genetic Predisposition to Disease...) : Toll-like receptor 11 ( TLR11 ) recognizes T. gondii profilin ( TgPRF ) and is required for interleukin-12 production and induction of immune responses that limit cyst burden in Toxoplasma gondii infected mice
Schamber-Reis et al., J Biol Chem 2013 (Disease Resistance...) : Altogether, our results indicate the redundant and essential role of nucleic acid sensing TLR3, TLR7 and TLR9 in inducing interleukin 12, development of a T1 response, and resistance to L. major infection in resistant C57BL/6 mice
Wu et al., PloS one 2013 : We showed that the hADSCs expressed Toll-like Receptors (TLR) 1, TLR2, TLR3, TLR4 , and TLR6 and that lipopolysaccharide (LPS) significantly induced the production of pro-inflammatory cytokines ( Cyclooxygenase-2 (Cox-2), Interleukin-1ß (IL-1ß), Interleukin-6 (IL-6), and Interleukin-8 (IL-8) )
Herath et al., PloS one 2013 (MAP Kinase Signaling System) : METHODOLOGYPRINCIPAL FINDINGS : This study systematically investigated the effects of P. gingivalis LPS1435/1449 and LPS1690 on the expression of TLR2 and TLR4 signal transduction and the activation of pro-inflammatory cytokines IL-6 and IL-8 in human gingival fibroblasts ( HGFs )
Brancato et al., Wound Repair Regen 2013 (Disease Progression...) : The accumulation of CCL2, CX3CL1, tumor necrosis factor-a, interleukin (IL)-6 , IL-10, IL-12, and interferon-? in wound fluids was not TLR4 dependent