British Medical Bulletin Advance Access originally published online on October 17, 2008
British Medical Bulletin 2008 88(1):95-113; doi:10.1093/bmb/ldn038
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Host-bacteria interaction in inflammatory bowel disease
Division of Gastroenterology, School of Clinical Sciences, University of Liverpool, Crown Street, Liverpool, L69 3BX, UK
* Correspondence to: Dr B. J. Campbell, School of Clinical Sciences, University of Liverpool, Nuffield Building, Crown Street, Liverpool L69 3BX, UK. E-mail: b.j.campbell{at}liverpool.ac.uk
Introduction/background: Inflammatory bowel disease (IBD) results from complex interactions between: host genome, immune system, mucosa, bacteria, and environment.
Sources of data: Review of PubMed database using search terms bacteria and inflammatory bowel disease and genetics and inflammatory bowel disease. PubMed related reference feature and references from retrieved articles were examined.
Areas of agreement: IBD results from interaction between the microbiota of the gut and the immune system. Key gene defects associated with IBD are involved in bacterial recognition and processing. The environment at least modifies and may determine pathogenesis.
Areas of controversy: It has been disputed whether the primary defect in IBD is immunological or bacterial, and which bacteria are key.
Growing points/areas for research: M cells, the specialized epithelial cells that overlie Peyer's patches, are a major interface between gut bacteria and the immune system. Improved understanding is needed of the bacteria involved in IBD pathogenesis, their genotypes and phenotypes, their portal of entry and their mechanism for escaping attack from the immune system. Bacterial ligands involved in bacteria–epithelial adhesion are emerging, and molecular techniques are rapidly increasing our knowledge of the human intestinal microbiota.
Keywords: Crohn's disease ulcerative colitis Escherichia coli macrophage autophagy M cell
Accepted for publication September 24, 2008.
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