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The recently published article by Gadaleta and co-workers1 has demonstrated that activation of the bile acid (BA) nuclear receptor, Farnesoid X receptor α (FXR), affords multi-level protection against intestinal inflammation and inflammatory bowel disease (IBD) in mice. Of the numerous avenues of research into IBD diagnosis and treatment that are opened by these findings, the questions posed by Gadaleta and co-workers regarding the contribution of gut bacteria to FXR modulation and aetiology of IBD are of particular significance.
Bacteria resident in the human gastrointestinal tract collectively encode a distributed pathway of BA modification, the products of which are the natural ligands for FXR,2 and there is growing appreciation that this may be a key activity through which the gut microbiota integrates factors relating to diet and mucosal inflammation, to initiate or exacerbate disease.3 These modified BAs display altered binding profiles for BA receptors, with several secondary BAs being among the most potent agonists. Moreover, microbial transformation could also influence BA bioavailability for …