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Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation.

ABSTRACT: Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their colonization. However, health conditions such as inflammatory bowel disease (IBD) are associated with a reduced mucus layer, potentially leading to dysbiosis associated with this disease. We characterize the capability of commensal species to cleave and transport mucin-associated monosaccharides and identify several Clostridiales members that utilize intestinal mucins. One such mucin utilizer, Peptostreptococcus russellii, reduces susceptibility to epithelial injury in mice. Several Peptostreptococcus species contain a gene cluster enabling production of the tryptophan metabolite indoleacrylic acid (IA), which promotes intestinal epithelial barrier function and mitigates inflammatory responses. Furthermore, metagenomic analysis of human stool samples reveals that the genetic capability of microbes to utilize mucins and metabolize tryptophan is diminished in IBD patients. Our data suggest that stimulating IA production could promote anti-inflammatory responses and have therapeutic benefits.

SUBMITTER: Wlodarska M

PROVIDER: S-EPMC5672633 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation.

Wlodarska Marta M Luo Chengwei C Kolde Raivo R d'Hennezel Eva E Annand John W JW Heim Cortney E CE Krastel Philipp P Schmitt Esther K EK Omar Abdifatah S AS Creasey Elizabeth A EA Garner Ashley L AL Mohammadi Sina S O'Connell Daniel J DJ Abubucker Sahar S Arthur Timothy D TD Franzosa Eric A EA Huttenhower Curtis C Murphy Leon O LO Haiser Henry J HJ Vlamakis Hera H Porter Jeffrey A JA Xavier Ramnik J RJ

Cell host & microbe 20170701 1

Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their colonization. However, health conditions such as inflammatory bowel disease (IBD) are associated with a reduced mucus layer, potentially leading to dysbiosis associated with this disease. We characterize the capability of commensal species to cleave and transport mucin-associated monosaccharides and identify several Clostridiales members that ...[more]

PMID: 28704649

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Project description:Dysregulated immune responses to commensal intestinal bacteria, including Escherichia coli, contribute to the development of inflammatory bowel diseases (IBDs) and experimental colitis. Reciprocally, E. coli responds to chronic intestinal inflammation by upregulating expression of stress response genes, including gadA and gadB. GadAB encode glutamate decarboxylase and protect E. coli from the toxic effects of low pH and fermentation acids, factors present in the intestinal lumen in patients with active IBDs. We hypothesized that E. coli upregulates gadAB during inflammation to enhance its survival and virulence. Using real-time PCR, we determined gadAB expression in luminal E. coli from ex-germfree wild-type (WT) and interleukin-10 (IL-10) knockout (KO) (IL-10(-/-)) mice selectively colonized with a commensal E. coli isolate (NC101) that causes colitis in KO mice in isolation or in combination with 7 other commensal intestinal bacterial strains. E. coli survival and host inflammatory responses were measured in WT and KO mice colonized with NC101 or a mutant lacking the gadAB genes (NC101?gadAB). The susceptibility of NC101 and NC101?gadAB to killing by host antimicrobial peptides and their translocation across intestinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, respectively. We show that expression of gadAB in luminal E. coli increases proportionately with intestinal inflammation in KO mice and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but decreases bacterial transmigration across intestinal epithelial cells, colonic inflammation, and mucosal immune responses. Chronic intestinal inflammation upregulates acid tolerance pathways in commensal E. coli isolates, which, contrary to our original hypothesis, limits their survival and colitogenic potential. Further investigation of microbial adaptation to immune-mediated inflammation may provide novel insights into the pathogenesis and treatment of IBDs.

Dataset Information

Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation.

Publications

Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation.

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