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COMMENTARY |
| Escherichia coli in IBD |
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, Crohns 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 Crohns disease-associated gene NOD2/CARD15 is a receptor for bacterial cell-wall peptidoglycan, the common presence of circulating anti-bacterial antibodies in Crohns 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 5001000 bacterial species2 and around 80% of these have yet to be cultured.3 There is
Relevant Article
Gut 2007 56: 669-675.
This article has been cited by other articles:
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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] |
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