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Letter to the editor regarding the report of Duboc et al: connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel disease
  1. Mitchell L Jones1,2,
  2. Christopher J Martoni2,
  3. Satya Prakash1,2
  1. 1Biomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, McGill University, Montreal, Quebec, Canada
  2. 2Micropharma Limited, Montreal, Quebec, Canada
  1. Correspondence to Professor Satya Prakash, Biomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering and Physiology, Artificial Cells and Organs Research Centre, Faculty of Medicine, McGill University, 3775 University Street, Montreal, QC, Canada H3A 2B4; satya.prakash{at}mcgill.ca

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We read with interest the informative and required investigation of bile-acid dysmetabolism, dysbiosis and inflammation in inflammatory bowel diseases (IBD) by Duboc et al.1 The paper suggests that a characteristic finding of IBD is reduced faecal secondary bile acids (BA), increased conjugated BA and increased sulphated BA.1 The authors link the luminal dysmetabolism of BA to dysbiosis, and the loss of microbiota deconjugation, transformation and desulphation enzymatic functions.1 The authors report convincing evidence demonstrating that a decrease in bacteria-bearing bile salt hydrolase (BSH) activities may be involved in the increase in conjugated BA remaining in the faeces, and show that germ-free mice have a similar loss of microbiota enzymatic function and display similar faecal BA irregularities.1 In addition to their role in dietary lipid absorption, BA are signalling modules activating nuclear receptors, including the farnesoid-X-receptor, the constitutive androstane receptor, the pregnane-X-receptor and the vitamin D receptor (VDR), as well as the …

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