Inflammatory bowel disease: Epidemiology, pathogenesis, and therapeutic opportunities

Stephen B. Hanauer*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

686 Scopus citations

Abstract

Ulcerative colitis (UC) and Crohn's disease (CD), the primary constituents of inflammatory bowel disease (IBD), are precipitated by a complex interaction of environmental, genetic, and immunoregulatory factors. Higher rates of IBD are seen in northern, industrialized countries, with greater prevalence among Caucasians and Ashkenazic Jews. Racial gaps are closing, indicating that environmental factors may play a role. IBD is multigenic, with the most clearly established genetic link between certain NOD2 variants and CD. Regardless of the underlying genetic predisposition, a growing body of data implicates a dysfunctional mucosal immune response to commensal bacteria in the pathogenesis of IBD, especially CD. Possible triggers include a chronic inflammatory response precipitated by infection with a particular pathogen or virus or a defective mucosal barrier. The characteristic inflammatory response begins with an infiltration of neutrophils and macrophages, which then release chemokines and cytokines. These in turn exacerbate the dysfunctional immune response and activate either TH1 or TH2 cells in the gut mucosa, respectively associated with CD and, less conclusively, with UC. Elucidation of immunological and genetic factors indicate multiple points at which the inflammatory cascade may be interrupted, yielding the possibility of precise, targeted therapies for IBD.

Original languageEnglish (US)
Pages (from-to)S3-S9
JournalInflammatory bowel diseases
Volume12
Issue number5 SUPPL. 1
DOIs
StatePublished - Jan 2006

Keywords

  • Commensal bacteria
  • Crohn's disease
  • Immunoregulatory defects
  • Inflammatory bowel disease
  • Ulcerative colitis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Gastroenterology

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