| http://purl.uniprot.org/citations/17475882 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17475882 | http://www.w3.org/2000/01/rdf-schema#comment | "Commensal 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."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.178.10.6522"xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/author | "Kim J.S."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/author | "Jobin C."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/author | "Magness S.T."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/author | "Muhlbauer M."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/author | "Karrasch T."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/pages | "6522-6532"xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/title | "Gnotobiotic IL-10-/-;NF-kappa B(EGFP) mice reveal the critical role of TLR/NF-kappa B signaling in commensal bacteria-induced colitis."xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://purl.uniprot.org/core/volume | "178"xsd:string |
| http://purl.uniprot.org/citations/17475882 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17475882 |
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| http://purl.uniprot.org/uniprot/#_A0A7R8GUQ3-mappedCitation-17475882 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17475882 |
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| http://purl.uniprot.org/uniprot/#_P00493-mappedCitation-17475882 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17475882 |
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