The commensal microbiota and enteropathogens in the pathogenesis of inflammatory bowel diseases

Gastroenterology. 2011 May;140(6):1720-28. doi: 10.1053/j.gastro.2011.01.054.


Intestinal inflammation arises from abnormal host-microbe interactions. The perturbations of homeostatic coexistence involve host genetic factors, barrier function, innate and adaptive immunity, as well as qualitative and quantitative changes in the composition of the microbiota. Dysbiosis toward selected micro-organisms and decreased complexity of commensal bacteria have been observed in patients with Crohn's disease and ulcerative colitis, but it is not clear whether the dysbiosis contributes to development of inflammatory bowel disease or is instead a consequence of the disease. Pathogens with virulence factors that allow them to breach the intestinal barrier and induce chronic inflammation might mediate the pathogenesis of these diseases. To identify new therapeutic approaches for inflammatory bowel disease, it is important to identify host susceptibility factors involved in the control of microbial infection, characterize potential pathogens, and eliminate them or block the expression of their virulence factors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Infections*
  • Colitis, Ulcerative / genetics
  • Colitis, Ulcerative / microbiology*
  • Crohn Disease / genetics
  • Crohn Disease / microbiology*
  • Genetic Predisposition to Disease
  • Humans
  • Intestines / microbiology*
  • Mycobacterium avium subsp. paratuberculosis
  • Paratuberculosis