Bile Acid-Related Regulation of Mucosal Inflammation and Intestinal Motility: From Pathogenesis to Therapeutic Application in IBD and Microscopic Colitis

Nutrients. 2022 Jun 27;14(13):2664. doi: 10.3390/nu14132664.


Inflammatory bowel diseases (IBD) and microscopic colitis are chronic immune-mediated inflammatory disorders that affect the gastroenterological tract and arise from a complex interaction between the host's genetic risk factors, environmental factors, and gut microbiota dysbiosis. The precise mechanistic pathways interlinking the intestinal mucosa homeostasis, the immunological tolerance, and the gut microbiota are still crucial topics for research. We decided to deeply analyze the role of bile acids in these complex interactions and their metabolism in the modulation of gut microbiota, and thus intestinal mucosa inflammation. Recent metabolomics studies revealed a significant defect in bile acid metabolism in IBD patients, with an increase in primary bile acids and a reduction in secondary bile acids. In this review, we explore the evidence linking bile acid metabolites with the immunological pathways involved in IBD pathogenesis, including apoptosis and inflammasome activation. Furthermore, we summarize the principal etiopathogenetic mechanisms of different types of bile acid-induced diarrhea (BAD) and its main novel diagnostic approaches. Finally, we discuss the role of bile acid in current and possible future state-of-the-art therapeutic strategies for both IBD and BAD.

Keywords: bile acid-induced diarrhea; bile acids; gut microbiome; inflammatory bowel diseases; microscopic colitis.

Publication types

  • Review

MeSH terms

  • Bile Acids and Salts / metabolism
  • Colitis, Microscopic* / metabolism
  • Colitis, Microscopic* / pathology
  • Gastrointestinal Motility
  • Humans
  • Inflammation / metabolism
  • Inflammatory Bowel Diseases* / metabolism
  • Intestinal Mucosa / metabolism
  • Mucositis* / metabolism


  • Bile Acids and Salts

Grants and funding

This research received no external funding.