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Review article

Host–bacterial interactions in inflammatory bowel disease

Yashwant R. MAHIDA, Vivien E. ROLFE
Clinical Science Oct 01, 2004, 107 (4) 331-341; DOI: 10.1042/CS20040136
Yashwant R. MAHIDA
Institute of Infection, Immunity and Inflammation, University Hospital, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH, U.K.
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  • For correspondence: yash.mahida@nottingham.ac.uk
Vivien E. ROLFE
Institute of Infection, Immunity and Inflammation, University Hospital, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH, U.K.
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Abstract

Large numbers of different bacterial species are resident in the lumen of the distal gastrointestinal tract. The normal intestinal host–microbial interactions are not well understood, but the relationship is generally believed to be either mutually beneficial or beneficial to one without disadvantage to the other. Animal model and clinical studies suggest that IBD (inflammatory bowel disease) may develop in a susceptible individual when the normal host–bacterial relationship is dysregulated. In addition to rodent models, this article reviews studies that have investigated the cellular and molecular mechanisms of interactions between intestinal mucosal cells and the resident luminal bacteria in healthy individuals and patients with ulcerative colitis and Crohn's disease. Mechanisms by which the intestinal mucosa is able to avoid pro-inflammatory responses to commensal bacteria (and their products) but able to respond appropriately to luminal pathogens is currently an area of active investigation. Such studies are beginning to provide important clues regarding possible alterations in the mucosa that lead to the development of pro-inflammatory responses to resident bacteria in patients with IBD. Approaches to alter the intestinal microflora for therapeutic purposes and their potential mechanisms of action are also discussed.

  • Crohn's disease
  • host–bacterial interaction
  • inflammatory bowel disease
  • mucosa
  • probiotics
  • therapeutics
  • ulcerative colitis

Abbreviations: IBD, inflammatory bowel disease; IL, interleukin; LPS, lipopolysaccharide; NF-κB, nuclear factor-κB; PAMP, pathogen-associated molecular pattern; sIgA, secretory IgA; TLR, Toll-like receptor; TGF-β, transforming growth factor-β

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October 2004

Volume: 107 Issue: 4

Clinical Science: 107 (4)
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Host–bacterial interactions in inflammatory bowel disease
Yashwant R. MAHIDA, Vivien E. ROLFE
Clinical Science Oct 2004, 107 (4) 331-341; DOI: 10.1042/CS20040136
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Host–bacterial interactions in inflammatory bowel disease
Yashwant R. MAHIDA, Vivien E. ROLFE
Clinical Science Oct 2004, 107 (4) 331-341; DOI: 10.1042/CS20040136

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  • Article
    • Abstract
    • INTRODUCTION
    • NORMAL HOST–BACTERIAL RELATIONSHIP
    • ROLE OF BACTERIA IN THE PATHOGENESIS OF IBD
    • MANIPULATION OF INTESTINAL BACTERIA FOR THERAPEUTIC PURPOSES
    • CONCLUSIONS
    • References
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Keywords

Crohn's disease
host–bacterial interaction
inflammatory bowel disease
mucosa
probiotics
therapeutics
ulcerative colitis

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