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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
DC Field | Value | Language |
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dc.contributor.author | Karrasch, Thomas | - |
dc.contributor.author | Kim, Joo-Sung | - |
dc.contributor.author | Muhlbauer, Marcus | - |
dc.contributor.author | Magness, Scott T | - |
dc.contributor.author | Jobin, Christian | - |
dc.date.accessioned | 2010-01-12T02:18:59Z | - |
dc.date.available | 2010-01-12T02:18:59Z | - |
dc.date.issued | 2007-05-04 | - |
dc.identifier.citation | J Immunol. 2007 May 15;178(10):6522-32. | en |
dc.identifier.issn | 0022-1767 (Print) | - |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17475882 | - |
dc.identifier.uri | https://hdl.handle.net/10371/29588 | - |
dc.description.abstract | 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. | en |
dc.language.iso | en | en |
dc.publisher | American Association of Immunologists | en |
dc.subject | Animals | en |
dc.subject | Colitis/genetics/*immunology/pathology | en |
dc.subject | Enterococcus faecalis/immunology | en |
dc.subject | Escherichia coli Infections/genetics/immunology/pathology | en |
dc.subject | Female | en |
dc.subject | Genes, Reporter | en |
dc.subject | Germ-Free Life/*immunology | en |
dc.subject | Gram-Positive Bacterial Infections/genetics/immunology/pathology | en |
dc.subject | Green Fluorescent Proteins/biosynthesis/*genetics | en |
dc.subject | Interleukin-10/*deficiency/*genetics/physiology | en |
dc.subject | Male | en |
dc.subject | Mice | en |
dc.subject | Mice, Inbred C57BL | en |
dc.subject | Mice, Knockout | en |
dc.subject | Mice, Mutant Strains | en |
dc.subject | NF-kappa B/*genetics/physiology | en |
dc.subject | Signal Transduction/genetics/*immunology | en |
dc.subject | Toll-Like Receptors/*physiology | en |
dc.title | Gnotobiotic IL-10-/-;NF-kappa B(EGFP) mice reveal the critical role of TLR/NF-kappa B signaling in commensal bacteria-induced colitis | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 김주성 | - |
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