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Formylpeptide receptor-2 contributes to colonic epithelial homeostasis, inflammation, and tumorigenesis.


ABSTRACT: Commensal bacteria and their products provide beneficial effects to the mammalian gut by stimulating epithelial cell turnover and enhancing wound healing, without activating overt inflammation. We hypothesized that N-formylpeptide receptors, which bind bacterial N-formylpeptides and are expressed by intestinal epithelial cells, may contribute to these processes. Here we report that formylpeptide receptor-2 (FPR2), which we show is expressed on the apical and lateral membranes of colonic crypt epithelial cells, mediates N-formylpeptide-dependent epithelial cell proliferation and renewal. Colonic epithelial cells in FPR2-deficient mice displayed defects in commensal bacterium-dependent homeostasis as shown by the absence of responses to N-formylpeptide stimulation, shortened colonic crypts, reduced acute inflammatory responses to dextran sulfate sodium (DSS) challenge, delayed mucosal restoration after injury, and increased azoxymethane-induced tumorigenesis. These results indicate that FPR2 is critical in mediating homeostasis, inflammation, and epithelial repair processes in the colon.

SUBMITTER: Chen K 

PROVIDER: S-EPMC3613917 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature

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Formylpeptide receptor-2 contributes to colonic epithelial homeostasis, inflammation, and tumorigenesis.

Chen Keqiang K   Liu Mingyong M   Liu Ying Y   Yoshimura Teizo T   Shen Wei W   Le Yingying Y   Durum Scott S   Gong Wanghua W   Wang Chunyan C   Gao Ji-Liang JL   Murphy Philip M PM   Wang Ji Ming JM  

The Journal of clinical investigation 20130401 4


Commensal bacteria and their products provide beneficial effects to the mammalian gut by stimulating epithelial cell turnover and enhancing wound healing, without activating overt inflammation. We hypothesized that N-formylpeptide receptors, which bind bacterial N-formylpeptides and are expressed by intestinal epithelial cells, may contribute to these processes. Here we report that formylpeptide receptor-2 (FPR2), which we show is expressed on the apical and lateral membranes of colonic crypt ep  ...[more]

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