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IBS‐induced constipation alters gut microbiota stability leading to intestinal transit time changes in the host
Author(s) -
Touw Ketrija,
Nadimpalli Anuradha,
Hubert Nathaniel,
Leone Vanessa,
Kashyap Purna,
Chang Eugene
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1027.8
Subject(s) - dysbiosis , butyrate , irritable bowel syndrome , gut flora , feces , bacteroides , bacteroidetes , microbiology and biotechnology , firmicutes , medicine , biology , immunology , bacteria , food science , genetics , 16s ribosomal rna , fermentation
Pathogenesis of Irritable Bowel Syndrome (IBS) is multifactorial, and gut microbes are sought to play a role in development and progression of disease. In this study we examined how constipation‐predominant Irritable Bowel Syndrome (IBS‐C) microbiota affect host intestinal transit and signaling pathways. To determine IBS‐C dysbiosis effects on the host, we introduced fecal microbiota from constipated mice to germ‐free recipients. Recipient mice of IBS‐C microbiota developed delayed GI transit time when compared to controls. Bacterial DNA analysis by HiSeq sequencing showed significant increase in Bacteroides uniformis , Bacteroides ovatus and Parabacteroides distasonis species from Bacteroidetes phylum in constipated mice. Fecal microbiota metabolic potential was measured with tetrazolium dye assay and showed significant differences between recipients of control and IBS‐C microbiota. Microbial metabolites such as short chain fatty acids (SCFA) are known to alter intestinal transit. SCFA levels in cecal contents of recipeints were measured by GC‐MS, and showed lower butyrate, propionate and acetate concentration in IBS‐C mice when compared to controls. To determine contractile properties of intestine after introduction of control and IBS‐C microbiota, we stimulated colonic rings with carbachol and KCl, and observed hypercontractility in IBS‐C microbiota recipients. To determine mechanism for delayed GI transit we analyzed colon tissues in fecal microbiota recipients by qRT‐PCR, and determined dysregulated neuromediator pathways. Overall, these results suggest that IBS‐C dysbiosis contributes to development of delayed transit time through microbial metabolite production and changes in colonic contractile properties. Support or Funding Information R01 DK097268 and T32 DK007074