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- Title
Formylpeptide receptor-2 contributes to colonic epithelial homeostasis, inflammation, and tumorigenesis.
- Authors
Chen, Keqiang; Mingyong Liu; Ying Liu; Yoshimura, Teizo; Wei Shen; Yingying Le; Durum, Scott; Wanghua Gong; Chunyan Wang; Ji-Liang Gao; Murphy, Philip M.; Ji Ming Wang
- 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.
- Subjects
BACTERIA; EPITHELIAL cells; WOUND healing; FORMYL peptide receptors; CELL proliferation; HOMEOSTASIS; INFLAMMATION; CARCINOGENESIS
- Publication
Journal of Clinical Investigation, 2013, Vol 123, Issue 4, p1694
- ISSN
0021-9738
- Publication type
Article
- DOI
10.1172/JCI65569