The pathogenesis of inflammatory bowel disease (IBD) involves an interaction between host susceptibility (which is partly genetically determined), mucosal immunity and the intestinal milieu. Micro-organisms have physiological effects on mucosal structure, epithelial turnover, the intestinal immune cells and, thus, on many intestinal functions. Toll-like receptors and nucleotide oligomerisation-binding domain proteins in host cells recognise specific bacterial molecules and modify the immune response. Human studies have repeatedly shown that the microbiota of patients with IBD differs from that of controls and is unstable, both in the intestinal lumen and at the surface of the mucosa. A single pathogen has not been identified, but potentially pro-inflammatory micro-organisms have been found in samples from IBD patients more often than from healthy controls. These include Mycobacterium paratuberculosis, and enteroadherent and invasive Escherichia coli in Crohn’s disease (CD). Ecological descriptions of the microbiota present in patients with IBD (either in the faeces or adherent to the mucosa) have repeatedly reported a decrease in usually dominant bacteria, especially those from the dominant phylum Firmicutes. A decrease in the biodiversity of Firmicutes has been observed in CD, while a recent study has shown that a decrease in Firmicutes, especially Faecalibacterium prausnitzii, was associated with CD and the post-operative recurrence of CD lesions in the ileum. Taken together, these results suggest that dysbiosis, or an imbalance within the (dominant) intestinal microbiota, may favour IBD.

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