Ursodeoxycholic acid and its taurine/glycine conjugated species reduce colitogenic dysbiosis and equally suppress experimental colitis in mice.

2.50
Hdl Handle:
http://hdl.handle.net/10033/620832
Title:
Ursodeoxycholic acid and its taurine/glycine conjugated species reduce colitogenic dysbiosis and equally suppress experimental colitis in mice.
Authors:
Van den Bossche, Lien; Hindryckx, Pieter; Devisscher, Lindsey; Devriese, Sarah; Van Welden, Sophie; Holvoet, Tom; Vilchez-Vargas, Ramiro; Vital, Marius ( 0000-0003-4185-3475 ) ; Pieper, Dietmar H; Vanden Bussche, Julie; Vanhaecke, Lynn; Van de Wiele, Tom; De Vos, Martine; Laukens, Debby
Abstract:
The promising results with secondary bile acids in experimental colitis suggest that they may represent an attractive and safe class of drugs for the treatment of inflammatory bowel diseases (IBD). However, the exact mechanism by which bile acid therapy confers protection from colitogenesis is currently unknown. Since the gut microbiota plays a crucial role in the pathogenesis of IBD, and exogenous bile acid administration may affect the community structure of the microbiota, we examined the impact of the secondary bile acid ursodeoxycholic acid (UDCA) and its taurine/glycine conjugates on the fecal microbial community structure during experimental colitis. Daily oral administration of UDCA, tauroursodeoxycholic acid (TUDCA) or glycoursodeoxycholic acid (GUDCA) equally lowered the severity of dextran sodium sulfate-induced colitis in mice, as evidenced by reduced body weight loss, colonic shortening and expression of inflammatory cytokines. Illumina sequencing demonstrated that bile acid therapy during colitis did not restore fecal bacterial richness and diversity. However, bile acid therapy normalized the colitis-associated increased ratio of Firmicutes to Bacteroidetes Interestingly, administration of bile acids prevented the loss of Clostridium cluster XIVa and increased the abundance of Akkermansia muciniphila, bacterial species known to be particularly decreased in IBD patients. We conclude that UDCA, which is an FDA-approved drug for cholestatic liver disorders, could be an attractive treatment option to reduce dysbiosis and improve inflammation in human IBD.
Affiliation:
Helmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.
Citation:
Ursodeoxycholic acid and its taurine/glycine conjugated species reduce colitogenic dysbiosis and equally suppress experimental colitis in mice. 2017 Appl. Environ. Microbiol.
Journal:
Applied and environmental microbiology
Issue Date:
23-Jan-2017
URI:
http://hdl.handle.net/10033/620832
DOI:
10.1128/AEM.02766-16
PubMed ID:
28115375
Type:
Article
Language:
en
ISSN:
1098-5336
Appears in Collections:
publications of the research group microbial interactions and processes (MINP)

Full metadata record

DC FieldValue Language
dc.contributor.authorVan den Bossche, Lienen
dc.contributor.authorHindryckx, Pieteren
dc.contributor.authorDevisscher, Lindseyen
dc.contributor.authorDevriese, Sarahen
dc.contributor.authorVan Welden, Sophieen
dc.contributor.authorHolvoet, Tomen
dc.contributor.authorVilchez-Vargas, Ramiroen
dc.contributor.authorVital, Mariusen
dc.contributor.authorPieper, Dietmar Hen
dc.contributor.authorVanden Bussche, Julieen
dc.contributor.authorVanhaecke, Lynnen
dc.contributor.authorVan de Wiele, Tomen
dc.contributor.authorDe Vos, Martineen
dc.contributor.authorLaukens, Debbyen
dc.date.accessioned2017-02-20T14:09:23Z-
dc.date.available2017-02-20T14:09:23Z-
dc.date.issued2017-01-23-
dc.identifier.citationUrsodeoxycholic acid and its taurine/glycine conjugated species reduce colitogenic dysbiosis and equally suppress experimental colitis in mice. 2017 Appl. Environ. Microbiol.en
dc.identifier.issn1098-5336-
dc.identifier.pmid28115375-
dc.identifier.doi10.1128/AEM.02766-16-
dc.identifier.urihttp://hdl.handle.net/10033/620832-
dc.description.abstractThe promising results with secondary bile acids in experimental colitis suggest that they may represent an attractive and safe class of drugs for the treatment of inflammatory bowel diseases (IBD). However, the exact mechanism by which bile acid therapy confers protection from colitogenesis is currently unknown. Since the gut microbiota plays a crucial role in the pathogenesis of IBD, and exogenous bile acid administration may affect the community structure of the microbiota, we examined the impact of the secondary bile acid ursodeoxycholic acid (UDCA) and its taurine/glycine conjugates on the fecal microbial community structure during experimental colitis. Daily oral administration of UDCA, tauroursodeoxycholic acid (TUDCA) or glycoursodeoxycholic acid (GUDCA) equally lowered the severity of dextran sodium sulfate-induced colitis in mice, as evidenced by reduced body weight loss, colonic shortening and expression of inflammatory cytokines. Illumina sequencing demonstrated that bile acid therapy during colitis did not restore fecal bacterial richness and diversity. However, bile acid therapy normalized the colitis-associated increased ratio of Firmicutes to Bacteroidetes Interestingly, administration of bile acids prevented the loss of Clostridium cluster XIVa and increased the abundance of Akkermansia muciniphila, bacterial species known to be particularly decreased in IBD patients. We conclude that UDCA, which is an FDA-approved drug for cholestatic liver disorders, could be an attractive treatment option to reduce dysbiosis and improve inflammation in human IBD.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleUrsodeoxycholic acid and its taurine/glycine conjugated species reduce colitogenic dysbiosis and equally suppress experimental colitis in mice.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalApplied and environmental microbiologyen

Related articles on PubMed

This item is licensed under a Creative Commons License
Creative Commons
All Items in HZI are protected by copyright, with all rights reserved, unless otherwise indicated.