The role of bacteria in onset and perpetuation of inflammatory bowel disease

P Seksik, H Sokol, P Lepage, N Vasquez… - Alimentary …, 2006 - Wiley Online Library
P Seksik, H Sokol, P Lepage, N Vasquez, C Manichanh, I Mangin, P Pochart, J Doré…
Alimentary pharmacology & therapeutics, 2006Wiley Online Library
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 (eg probiotics,
CpG‐DNA) or selectively increasing some endogenous bacteria (eg using prebiotics).
Intervention studies were performed in patients or animal models of spontaneous or …
Summary
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.
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