| Literature DB >> 28384049 |
Shinsaku Okai1, Fumihito Usui1, Misa Ohta1, Hiroshi Mori2, Ken Kurokawa2, Satoshi Matsumoto3, Tamotsu Kato4, Eiji Miyauchi4, Hiroshi Ohno4,5,6, Reiko Shinkura1,7.
Abstract
Accumulating evidence suggests that dysbiosis plays a role in the pathogenesis of intestinal diseases including inflammatory bowel disease (IBD) as well as extra-intestinal disorders. As a modulator of the intestinal microbiota, we isolated a mouse monoclonal IgA antibody (clone W27) with high affinities for multiple commensal bacteria, but not for beneficial bacteria such as Lactobacillus casei (L. casei). Via specific recognition of an epitope in serine hydroxymethyltransferase (SHMT), a bacterial metabolic enzyme, W27 IgA selectively inhibited the in vitro growth of bound bacteria, including Escherichia coli (E. coli), while having no effect on unbound beneficial bacteria such as L. casei. By modulating the gut microbiota in vivo, oral administration of W27 IgA effectively prevented development of colitis in several mouse models. Here we discuss how intestinal IgA modulates the gut microbiota through recognition of SHMT.Entities:
Keywords: AID; IgA; dysbiosis; gut microbiota; inflammatory bowel disease; monoclonal antibody
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Year: 2017 PMID: 28384049 PMCID: PMC5628655 DOI: 10.1080/19490976.2017.1310357
Source DB: PubMed Journal: Gut Microbes ISSN: 1949-0976