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Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic conditions characterised by recurrent episodes of intestinal inflammation. It is widely accepted that genetic predisposition and environmental factors contribute to the onset and the development of IBD. Many host factors that influence the onset of IBD have been identified and mainly include genes that are involved in microbial recognition, like NOD2, or in the immune response to infection, like interleukin-23. By contrast, the search for a microbial cause of IBD has not led to definitive answers.
Trillions of microbes constitute the intestinal microbiota of healthy individuals. This ‘healthy microbiota’ is comprised of mostly anaerobes of the Bacteroidetes and Firmicutes phyla and maintains a healthy gut by boosting mucosal immunity and providing colonisation resistance to pathogens. By contrast, patients with IBD exhibit a marked dysbiosis characterised by an expansion of Proteobacteria, though it is not clear if bacteria of this phylum cause intestinal inflammation or if their proliferation is a consequence of inflammation.1
Evidence for Proteobacteria as a potential trigger of IBD has been deduced by cohort studies showing that inflammatory diarrhoea caused by either Salmonella species or Campylobacter species predisposes genetically susceptible individuals to developing IBD.2 One possible scenario is that in …