The intestinal microbiota is involved in the pathogenesis of inflammatory bowel disease. A reduction in the diversity of the intestinal microbiota as well as specific taxonomic and functional shifts have been reported in Crohn's disease and may play a central role in the inflammatory process. The aim was to systematically review recent developments in the structural and functional changes observed in the gastrointestinal microbiome in patients with Crohn's Disease.
Seventy-two abstracts were included in this review. The effects of host genetics, disease phenotype, and inflammatory bowel disease treatment on the gastrointestinal microbiome in Crohn's disease were reviewed, and taxonomic shifts in patients with early and established disease were described. The relative abundance of Bacteroidetes is increased and Firmicutes decreased in Crohn's disease compared with healthy controls. Enterobacteriaceae, specifically Eschericia coli, is enriched in Crohn's disease. Faecalibacterium prausnitzii is found at lower abundance in Crohn's disease and in those with postoperative recurrence. Observed functional changes include major shifts in oxidative stress pathways, a decrease in butanoate and propanoate metabolism gene expression, lower levels of butyrate, and other short-chain fatty acids, decreased carbohydrate metabolism, and decreased amino acid biosynthesis.
Changes in microbial composition and function have been described, although a causative role remains to be established. Larger, prospective, and longitudinal studies are required with deep interrogation of the microbiome if causality is to be determined, and refined microbial manipulation is to emerge as a focused therapy.
Article first published online 3 April 2015.
*Department of Gastroenterology, St Vincent's Hospital Melbourne, Australia;
†Department of Pathology, University of Melbourne, Australia;
‡Imperial College, London, United Kingdom; and
§Enteric Virus Group, Murdoch Children's Research Institute, Melbourne, Australia.
Reprints: Michael A. Kamm, MD, PhD, St Vincent's Hospital, Victoria Parade, Fitzroy 3065, Melbourne, Australia (e-mail: firstname.lastname@example.org).
The authors have no conflicts of interest to disclose.
Received January 03, 2015
Accepted February 03, 2015