Document Detail


Formylpeptide receptor-2 contributes to colonic epithelial homeostasis, inflammation, and tumorigenesis.
MedLine Citation:
PMID:  23454745     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Keqiang Chen; Mingyong Liu; Ying Liu; Teizo Yoshimura; Wei Shen; Yingying Le; Scott Durum; Wanghua Gong; Chunyan Wang; Ji-Liang Gao; Philip M Murphy; Ji Ming Wang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  123     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-05-09     Completed Date:  2013-05-20     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1694-704     Citation Subset:  AIM; IM    
Affiliation:
Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Proliferation
Cell Transformation, Neoplastic / metabolism*
Colitis / chemically induced,  metabolism*,  microbiology
Colon / pathology*
Colonic Neoplasms / metabolism*
Cytokines / genetics,  metabolism
Dextran Sulfate
Epithelial Cells / metabolism*,  pathology,  physiology
Gene Expression
Homeostasis
Inflammation Mediators / metabolism
Intestinal Mucosa / metabolism,  microbiology,  pathology
Ki-67 Antigen / metabolism
Mice
Mice, Knockout
Receptors, Formyl Peptide / genetics,  metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
HHSN261200800001E//PHS HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Fpr1 protein, mouse; 0/Inflammation Mediators; 0/Ki-67 Antigen; 0/Receptors, Formyl Peptide; 0/formyl peptide receptor 2, mouse; 9042-14-2/Dextran Sulfate
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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