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Gnotobiotic IL-10-/-;NF-kappa B(EGFP) mice reveal the critical role of TLR/NF-kappa B signaling in commensal bacteria-induced colitis

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dc.contributor.authorKarrasch, Thomas-
dc.contributor.authorKim, Joo-Sung-
dc.contributor.authorMuhlbauer, Marcus-
dc.contributor.authorMagness, Scott T-
dc.contributor.authorJobin, Christian-
dc.date.accessioned2010-01-12T02:18:59Z-
dc.date.available2010-01-12T02:18:59Z-
dc.date.issued2007-05-04-
dc.identifier.citationJ Immunol. 2007 May 15;178(10):6522-32.en
dc.identifier.issn0022-1767 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17475882-
dc.identifier.urihttps://hdl.handle.net/10371/29588-
dc.description.abstractCommensal bacteria and TLR signaling have been associated with the maintenance of intestinal homeostasis in dextran sodium sulfate-induced intestinal injury. The aim of this study was to determine the in vivo role of TLR/NF-kappaB activation in a model of commensal bacteria-induced T cell-mediated colitis. A NF-kappaB reporter gene mouse (NF-kappaBEGFP) (EGFP, enhanced GFP) was crossed to the colitogenic susceptible strain IL-10-/- and derived into germfree conditions using embryo-transfer technology. Germfree IL-10wt/wt;NF-kappaBEGFP and IL-10-/-;NF-kappaBEGFP mice (wt, wild type) were dual associated with the nonpathogenic commensal bacteria strains Enterococcus faecalis and Escherichia coli. EGFP was detected using macroimaging, confocal microscopy, and flow cytometry. IL-10-/-;MyD88-/- mice were used to assess E. faecalis/E. coli-induced TLR-dependent signaling and IL-23 gene expression. Dual-associated IL-10-/-;NF-kappaBEGFP mice developed severe inflammation by 7 wk. Macroscopic analysis showed elevated EGFP expression throughout the colon of bacteria-associated IL-10-/-;NF-kappaBEGFP mice. Confocal microscopy analysis revealed EGFP-positive enterocytes during the early phase of bacterial colonization (1 wk) in both IL-10wt/wt and IL-10-/- mice, while the signal shifted toward lamina propria T cells, dendritic cells, neutrophils, and macrophages in IL-10-/- mice during colitis (7 wk). The NF-kappaB inhibitor BAY 11-7085 attenuated E. faecalis/E. coli-induced EGFP expression and development of colitis. Additionally, E. faecalis/E. coli-induced NF-kappaB signaling and IL-23 gene expression were blocked in bone marrow-derived dendritic cells derived from IL-10-/-;MyD88-/- mice. We conclude that bacteria-induced experimental colitis involves the activation of TLR-induced NF-kappaB signaling derived mostly from mucosal immune cells. Blocking TLR-induced NF-kappaB activity may represent an attractive strategy to treat immune-mediated intestinal inflammation.en
dc.language.isoenen
dc.publisherAmerican Association of Immunologistsen
dc.subjectAnimalsen
dc.subjectColitis/genetics/*immunology/pathologyen
dc.subjectEnterococcus faecalis/immunologyen
dc.subjectEscherichia coli Infections/genetics/immunology/pathologyen
dc.subjectFemaleen
dc.subjectGenes, Reporteren
dc.subjectGerm-Free Life/*immunologyen
dc.subjectGram-Positive Bacterial Infections/genetics/immunology/pathologyen
dc.subjectGreen Fluorescent Proteins/biosynthesis/*geneticsen
dc.subjectInterleukin-10/*deficiency/*genetics/physiologyen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectMice, Knockouten
dc.subjectMice, Mutant Strainsen
dc.subjectNF-kappa B/*genetics/physiologyen
dc.subjectSignal Transduction/genetics/*immunologyen
dc.subjectToll-Like Receptors/*physiologyen
dc.titleGnotobiotic IL-10-/-;NF-kappa B(EGFP) mice reveal the critical role of TLR/NF-kappa B signaling in commensal bacteria-induced colitisen
dc.typeArticleen
dc.contributor.AlternativeAuthor김주성-
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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