Abstract：
:Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn's disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Carvalho FA,Koren O,Goodrich JK,Johansson ME,Nalbantoglu I,Aitken JD,Su Y,Chassaing B,Walters WA,González A,Clemente JC,Cullender TC,Barnich N,Darfeuille-Michaud A,Vijay-Kumar M,Knight R,Ley RE,Gewirtz ATdoi
10.1016/j.chom.2012.07.004subject
Has Abstractpub_date
2012-08-16 00:00:00pages
139-52issue
2eissn
1931-3128issn
1934-6069pii
S1931-3128(12)00227-2journal_volume
12pub_type
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