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This Article Full Text Full Text (PDF) All Versions of this Article: 295/6/G1139    most recent 90516.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Chichlowski, M. Articles by Hale, L. P. Search for Related Content PubMed PubMed Citation Articles by Chichlowski, M. Articles by Hale, L. P.

REVIEW

Bacterial-mucosal interactions in inflammatory bowel disease—an alliance gone bad

Department of Pathology, Duke University Medical Center, Durham, North Carolina

Submitted 26 August 2008 ; accepted in final form 14 October 2008

ABSTRACT

The complex interaction of genetic, microbial, and environmental factors may result in continuous activation of the mucosal immune system leading to inflammatory bowel disease (IBD). Most present treatments for IBD involve altering or suppressing the aberrant immune response; however, the role of the intestinal microbiota in the pathophysiology of IBD is becoming more evident. The epithelial layer is essential for the proper functioning of the gastrointestinal tract, and its increased permeability to the luminal antigens may lead to the inflammatory processes and mucosal damage observed in IBD. Factors affecting the efficacy of the epithelial barrier include presence of pathogenic bacteria (e.g., Helicobacter spp.), presence of probiotic bacteria, availability of selected nutrients, and others. Defective function of the mucosal barrier might facilitate the contact of bacterial antigens and adjuvants with innate and adaptive immune cells to generate prolonged inflammatory responses. This review will briefly describe the complex structure of the epithelial barrier in the context of bacterial-mucosal interactions observed in human IBD and mouse models of colitis.

enteric bacteria; permeability; inflammation

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