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IL8 — S100A8

Text-mined interactions from Literome

Selbach et al., Infect Immun 2002 : Induction of IL-8 secretion depended largely on the same set of genes but was independent of CagA and VirD4 ... Thus, CagA translocation and induction of IL-8 secretion are regulated by VirD4-CagA dependent and VirD4-CagA independent mechanisms, respectively
Fischer et al., Mol Microbiol 2001 (Translocation, Genetic) : Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island : essential genes for CagA translocation in host cells and induction of interleukin-8 ... Seventeen out of 27 genes were found to be absolutely essential for translocation of CagA into host cells and 14 out of 27 for the ability of Hp fully to induce transcription of IL-8 ... In contrast, the products of hp0520, hp0521, hp0534, hp0535, hp0536 and hp0543 are not necessary for either translocation of CagA or for IL-8 induction
Odenbreit et al., Int J Med Microbiol 2002 : CagA tyrosine phosphorylation and interleukin-8 induction by Helicobacter pylori are independent from alpAB, HopZ and bab group outer membrane proteins ... In this study, we investigated the influence of several outer membrane proteins associated with adherence on CagA translocation and IL-8 induction ... Despite this partial adherence defect, the alpAB mutation did not affect CagA translocation and IL-8 induction ... No causative linkage could be found between the production of the outer membrane proteins HopZ, OipA or seven additional outer membrane proteins and CagA translocation or IL-8 induction
Rohde et al., Mol Microbiol 2003 : Type I strains of Helicobacter pylori ( Hp ) use a type IV secretion system ( T4SS ), encoded by the cag pathogenicity island ( cag-PAI ), to deliver the bacterial protein CagA into eukaryotic cells and to induce interleukin-8 secretion
Brandt et al., Proc Natl Acad Sci U S A 2005 (Inflammation...) : Our results suggest that IL-8 release induced by CagA occurs via a Ras-->Raf -- > Mek -- > Erk -- > NF-kappaB signaling pathway in a Shp-2- and c-Met independent manner
Kim et al., Cell Microbiol 2006 : To determine the effect of Helicobacter pylori CagA expression on interleukin-8 (IL-8) induction in AGS cells, cagA and five of its fragments from strains 147A and 147C that vary in the 3 ' repeat region were cloned into the eukaryotic expression plasmid pSP65SRalpha ... Use of specific inhibitors indicates that Src kinase activation, and the mitogen activated protein ( MAP ) kinase and NF-kappaB pathways are the major intermediates for CagA effects on IL-8 induction, but the p38 MAP kinase pathway has little effect ... These results indicate a direct CagA effect on IL-8 induction by gastric epithelial cells, and indicate signal pathway loci that can be targeted for amelioration
Lai et al., Infect Immun 2008 : Upon cholesterol depletion, the distribution shifted to non-DRMs. Accordingly, the CagA induced hummingbird phenotype and interleukin-8 induction were blocked by cholesterol depletion
Cendron et al., J Mol Biol 2009 : The Helicobacter pylori CagD ( HP0545, Cag24 ) protein is essential for CagA translocation and maximal induction of interleukin-8 secretion
Lee et al., Dig Dis Sci 2011 : Transfection of CagA into gastric epithelial cells induced morphologic changes ( hummingbird phenotype ), ZO-1 mislocalization, and IL-8 production in gastric epithelial cells
Li et al., Biomed Environ Sci 2010 : In this study, we try to determine roles of CagA ( + ) strain in activating PI3K/Akt1 signaling pathway, and affecting expression of p21 ( WAF1/CIP1 ) and p27 ( KIP1 ), and also in releasing IL-8 in host cells ... Both the CagA ( + ) and CagA? H. pylori strains enabled AGS cells to produce close elevated levels of IL-8, and the LY294002 block resulted in unexpected elevations of IL-8 levels
Barry et al., PloS one 2011 (Gastritis...) : Difluoromethylornithine is a novel inhibitor of Helicobacter pylori growth, CagA translocation, and interleukin-8 induction
Shaffer et al., PLoS Pathog 2011 (Helicobacter Infections) : Deletion of these motifs results in abrogation of CagA translocation and IL-8 induction , and the C-terminal motifs of CagI and CagL are required for formation of pili
Lai et al., FEMS Microbiol Lett 2011 : Helicobacter pylori CagA mediated IL-8 induction in gastric epithelial cells is cholesterol dependent and requires the C-terminal tyrosine phosphorylation containing domain ... We found that disruption of the lipid rafts reduced the level of CagA translocation/phosphorylation as well as CagA mediated IL-8 secretion ... By CagA truncated mutagenesis, we identified that the CTD, rather than the N-terminal domain, was responsible for CagA tethering to the plasma membrane and association with detergent-resistant membranes, leading to CagA induced IL-8 promoter activity
Schelbergen et al., Arthritis Rheum 2012 (Osteoarthritis) : Stimulation of chondrocytes with S100A8 and S100A9 caused a strong up-regulation of catabolic markers ( MMPs 1, 3, 9, and 13, interleukin-6 [ IL-6 ], IL-8 , and monocyte chemotactic protein 1 ) and down-regulation of anabolic markers ( aggrecan and type II collagen ), thereby favoring cartilage breakdown
Abbas et al., Stroke 2012 (Carotid Artery Diseases...) : Our main findings were : ( 1 ) plasma levels of S100A12 were significantly higher in patients with carotid atherosclerosis compared with healthy control subjects with the highest levels in patients with the most recent symptoms ( ie, within 2 months ) ; ( 2 ) plasma levels of S100A8/S100A9 showed a modest increase in patients with symptoms in the previous 2 to 6 months but not in the other patients ; ( 3 ) mRNA levels of S100A8, S100A9, and S100A12 showed increased expression in atherosclerotic carotid plaques from patients with the most recent symptoms compared with the remaining patients ; ( 4 ) in THP-1 monocytes, activation of Toll-like receptors 2 and 4 increased mRNA levels of S100A8 , S100A9, and S10012 and interleukin-1ß , interferon ?, and releasate from thrombin activated platelets significantly enhanced the expression of S100A12
Pham et al., PloS one 2012 (Helicobacter Infections) : Using a marker-free gene deletion approach and genetic complementation, we show now that CagI is an essential component of the Cag type IV secretion apparatus for both CagA translocation and interleukin-8 induction
Kim et al., Biochem Biophys Res Commun 2012 (Colorectal Neoplasms...) : The upregulation of S100A8/A9 in tumor infiltrated myeloid cells could be triggered by IL-6 and IL-8 released from myofibroblasts, and myofibroblasts might induce the differentiation of myeloid cells into S100A8/9 expressing MDSCs or M2 macrophages in the CRC microenvironment
Crabtree et al., J Clin Pathol 1995 : These studies show that CagA is not the inducer of IL-8 secretion from gastric epithelial cells