The relationship between fecal bile acids and microbiome community structure in pediatric Crohn's disease

ISME J. 2020 Mar;14(3):702-713. doi: 10.1038/s41396-019-0560-3. Epub 2019 Dec 3.

Jessica Connors 1, Katherine A Dunn 2, Jennifer Allott 2, Robert Bandsma 3, Mohsin Rashid 1 4, Anthony R Otley 1 4, Joseph P Bielawski 2 5, Johan Van Limbergen 6 7 8


Author information

  • 1Division of Pediatric Gastroenterology & Nutrition, IWK Health Centre, Halifax, NS, Canada.
  • 2Department of Biology, Dalhousie University, Halifax, NS, Canada.
  • 3Division of Pediatric Gastroenterology, Hepatology & Nutrition, Hospital for Sick Children, Toronto, ON, Canada.
  • 4Department of Pediatrics, Dalhousie University, Halifax, NS, Canada.
  • 5Department of Mathematics & Statistics, Dalhousie University, Halifax, NS, Canada.
  • 6Department of Pediatrics, Dalhousie University, Halifax, NS, Canada. j.e.vanlimbergen@amsterdamumc.nl.
  • 7Division of Pediatric Gastroenterology & Nutrition, Emma Children's Hospital, Amsterdam University Medical Centers, Amsterdam, The Netherlands. j.e.vanlimbergen@amsterdamumc.nl.
  • 8Tytgat Institute for Liver and Intestinal Research, Amsterdam Gastroenterology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. j.e.vanlimbergen@amsterdamumc.nl.


Gut microbiome community structure is associated with Crohn's disease (CD) development and response to therapy. Bile acids (BAs) play a central role in modulating intestinal immune responses, and changes in gut bacterial communities can profoundly alter the intestinal BA pool. The liver synthesizes and conjugates primary bile acids (priBAs) that are then deconjugated, epimerized, and dehydroxylated by gut bacteria to produce secondary bile acids (secBAs). We investigated the relationship between the gut microbiome and the fecal BA pool in stool samples obtained from a well-characterized cohort of pediatric CD patients undergoing nutritional therapy to induce disease remission. We found that fecal BA composition was altered in a sub-group of CD patients who did not sustain remission. The microbial community structures associated with priBA and secBA-dominant profiles were distinct. In addition, the fecal BA concentrations were correlated with the abundance of distinct bacterial taxonomic groups. Finally, priBA dominant samples were associated with community-level decreases in enzymes for dehydroxylation but not deconjugation.

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