There is a widespread assumption that both of the major inflammatory bowel diseases, Crohn’s disease and ulcerative colitis, arise as a result of a host response to intestinal bacteria. Evidence to support this includes the involvement of non-pathogenic bacteria in the development of colitis in genetically altered animals, knowledge that the Crohn’s disease-associated gene NOD2/CARD15 is a receptor for bacterial cell-wall peptidoglycan, the common presence of circulating anti-bacterial antibodies in Crohn’s disease, and the role of known pathogens in precipitating relapse in ulcerative colitis.¹ We still need to know which bacteria are the culprits, where they are (intraluminal, intramucosal, intracellular) and whether there is an abnormal host response to “commensal” bacteria or whether the bacteria themselves have pathogenic features.

Study of the gut microbiota is not easy. The human gut contains 500–1000 bacterial species² and around 80% of these have yet to be cultured.³ There is growing evidence that the bacteria that are closely related to or adherent to the mucosa may be more relevant to mucosal inflammation than those in the faeces. Studies of the mucosa-associated bacteria are, however, affected by the method used. The colonic mucosa, unlike the small intestine, has a near-continuous mucus coat⁴ and bacteria adherent to the surface of this coat will differ in number and nature from those underneath the mucus. Moreover, the surface of the mucus layer, like the faeces, is likely to suit the growth predominantly of anaerobic bacteria, whereas mucus represents a significant barrier to oxygen diffusion,⁵ so the sub-mucus niche may be relatively well oxygenated by the underlying mucosa and more suitable for micro-aerophilic bacteria. We have found that aerobic culture of colonoscopic biopsies after removal of the mucus layer with dithiothreitol is often …