Inﬂ ammatory bowel diseases (IBD) are thought to develop as a result of an exaggerated immune response to the gut microbiota. Animal models of inﬂ ammation require bacteria to produce inﬂ ammation (Sartor 2004). Antibiotics are effective in Crohn’s disease (CD), pouchitis and ulcerative colitis (UC), and probiotics have therapeutic efﬁ cacy in pouchitis and UC (Sartor 2004). Diversion of the faecal stream from the inﬂ amed gut induces healing in CD, while re-infusion of intestinal content into surgically excluded ileum triggers early disease recurrence (D’Haens et al. 1998). These ﬁ ndings have helped establish that the gut microbiota is a key contributor to IBD pathogenesis, with disease more prevalent in genetically susceptible individuals (Jostins et al. 2012).