p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and enteritis.
about
Clostridium difficile toxins: mechanism of action and role in disease.Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal EffectsThe Role of Rho GTPases in Toxicity of Clostridium difficile ToxinsIn vivo physiological and transcriptional profiling reveals host responses to Clostridium difficile toxin A and toxin BImmune responses to Clostridium difficile infectionContribution of adenosine A(2B) receptors in Clostridium difficile intoxication and infection.Inhibition of Na+/H+ exchanger enhances low pH-induced L-selectin shedding and beta2-integrin surface expression in human neutrophils.Monocytes are highly sensitive to clostridium difficile toxin A-induced apoptotic and nonapoptotic cell deathRegulation of lipopolysaccharide-induced increases in neutrophil glucose uptake.The glucocorticoid receptor blocks P-TEFb recruitment by NFkappaB to effect promoter-specific transcriptional repression.Shigella flexneri Interactions with the Basolateral Membrane Domain of Polarized Model Intestinal Epithelium: Role of Lipopolysaccharide in Cell Invasion and in Activation of the Mitogen-Activated Protein Kinase ERKThe myxobacterial compounds spirangien a and spirangien M522 are potent inhibitors of IL-8 expression.Helicobacter pylori activates the early growth response 1 protein in gastric epithelial cellsMicrobes and microbial toxins: paradigms for microbial-mucosal interactions II. The integrated response of the intestine to Clostridium difficile toxins.Bacterial factors exploit eukaryotic Rho GTPase signaling cascades to promote invasion and proliferation within their host.Clostridium difficile toxin A decreases acetylation of tubulin, leading to microtubule depolymerization through activation of histone deacetylase 6, and this mediates acute inflammation.Alternate surfaces of transcriptional coregulator GRIP1 function in different glucocorticoid receptor activation and repression contexts.The roles of host and pathogen factors and the innate immune response in the pathogenesis of Clostridium difficile infection.Toll-like receptor 5 stimulation protects mice from acute Clostridium difficile colitis.RhoC GTPase overexpression modulates induction of angiogenic factors in breast cells.Regulation of the NK-1 receptor gene expression in human macrophage cells via an NF-kappa B site on its promoter.Role of microbiota and innate immunity in recurrent Clostridium difficile infection.The insect peptide coprisin prevents Clostridium difficile-mediated acute inflammation and mucosal damage through selective antimicrobial activity.Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeabilityRecurrent Clostridium difficile infection: From colonization to cure.The large clostridial toxins from Clostridium sordellii and C. difficile repress glucocorticoid receptor activity.Urocortin II mediates pro-inflammatory effects in human colonocytes via corticotropin-releasing hormone receptor 2alpha.Clostridium difficile-associated colitisClostridium difficile toxins: mediators of inflammation.Clostridium difficile colitis: pathogenesis and host defenceIntrarectal instillation of Clostridium difficile toxin A triggers colonic inflammation and tissue damage: development of a novel and efficient mouse model of Clostridium difficile toxin exposure.The intestinal microbiota dysbiosis and Clostridium difficile infection: is there a relationship with inflammatory bowel disease?Local injection of dsRNA targeting calcitonin receptor-like receptor (CLR) ameliorates Clostridium difficile toxin A-induced ileitisAPOL1 kidney disease risk variants cause cytotoxicity by depleting cellular potassium and inducing stress-activated protein kinases.MAPK-activated protein kinase 2 contributes to Clostridium difficile-associated inflammationThe ecology and pathobiology of Clostridium difficile infections: an interdisciplinary challengeFlavonoid naringenin: a potential immunomodulator for Chlamydia trachomatis inflammation.Human monoclonal antibodies against Clostridium difficile toxins A and B inhibit inflammatory and histologic responses to the toxins in human colon and peripheral blood monocytes.Markers of intestinal inflammation, not bacterial burden, correlate with clinical outcomes in Clostridium difficile infection.Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity.
P2860
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P2860
p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and enteritis.
description
2000 nî lūn-bûn
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2000 թուականի Ապրիլին հրատարակուած գիտական յօդուած
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2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
name
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@ast
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@en
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@nl
type
label
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@ast
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@en
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@nl
prefLabel
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@ast
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@en
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@nl
P2093
P2860
P356
P1476
p38 MAP kinase activation by C ...... L-8 production, and enteritis.
@en
P2093
A C Keates
C Pothoulakis
I Castagliuolo
J T LaMont
S Aboudola
P2860
P304
P356
10.1172/JCI7545
P407
P577
2000-04-01T00:00:00Z