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The role of Escherichia coli in inflammatory bowel disease

Correspondence to:
Correspondence to:
ProfessorJonathanRhodes
School of Clinical Sciences, University of Liverpool, Duncan Building, Daulby Street, Liverpool L69 3GA; rhodesjm@liverpool.ac.uk

The first 150 words of the full text of this article appear below.

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 . . . [Full text of this article]

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High prevalence of Escherichia coli belonging to the B2+D phylogenetic group in inflammatory bowel disease

Roman Kotlowski, Charles N Bernstein, Shadi Sepehri, and Denis O Krause
Gut 2007 56: 669-675. [Abstract] [Full Text] [PDF]

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				J.-F. Colombel, A. J M Watson, and M. F Neurath The 10 remaining mysteries of inflammatory bowel disease Gut, April 1, 2008; 57(4): 429 - 433. [Full Text] [PDF]