Review article: the role of bacteria in onset and perpetuation of inflammatory bowel disease
Article first published online: 31 AUG 2006
Alimentary Pharmacology & Therapeutics
Special Issue: th New Approaches to the Detection and Management of Inflammatory Bowel Disease: From Genetic Testing to Treatment Strategies
Volume 24, Issue Supplement s3, pages 11–18, October 2006
How to Cite
SEKSIK, P., SOKOL, H., LEPAGE, P., VASQUEZ, N., MANICHANH, C., MANGIN, I., POCHART, P., DORÉ, J. and MARTEAU, P. (2006), Review article: the role of bacteria in onset and perpetuation of inflammatory bowel disease. Alimentary Pharmacology & Therapeutics, 24: 11–18. doi: 10.1111/j.1365-2036.2006.03053.x
- Issue published online: 31 AUG 2006
- Article first published online: 31 AUG 2006
- Publication data Submitted 28 June 2006 Accepted 28 June 2006
We review the evidence that strongly suggests a role of the intestinal microbiota in the onset and perpetuation of inflammatory bowel disease (IBD).
Experimental studies consisted of suppressing micro-organisms from the microbiota (using germ-free or gnotoxenic animals or antibiotics), introducing new micro-organisms or microbial components (e.g. probiotics, CpG-DNA) or selectively increasing some endogenous bacteria (e.g. using prebiotics).
Intervention studies were performed in patients or animal models of spontaneous or chemically-induced colitis.
Information was also obtained from observational studies that described the composition of the faecal and mucosal microbiota at various stages of the disease process and in controls. Many have used culture-independent techniques that identify bacteria based on the nucleic acid sequence of ribosomal RNA molecules. Microbiota in patients with IBD seem to be characterized by high concentrations of bacteria in contact with the mucosa, instability, the presence of high numbers of unusual bacteria and sometimes a reduction in the biodiversity.
Studies searching for a generalized or localized dysbiosis in IBD are discussed, as well as those trying to identify bacterial molecules and receptors, which may be implicated in triggering the inflammatory process.