Nitric oxide and chronic gut inflammation: controversies in inflammatory bowel disease

J Investig Med. 2002 Jul;50(4):272-83. doi: 10.2310/6650.2002.33281.


One of the most consistent and dramatic findings in both experimental and human inflammatory bowel disease (e.g., Crohn's disease, ulcerative colitis) is the enhanced expression of the inducible isoform of nitric oxide synthase (iNOS) and the sustained overproduction of the free radical nitric oxide (NO). The role that iNOS-derived NO plays in the pathophysiology of inflammatory bowel disease remains the subject of intense investigation and active debate. Although several different studies using a variety of animal models of acute and chronic gut inflammation suggest that NO may promote intestinal inflammation, an equally impressive number of investigations suggest that iNOS may play no role or may act to attenuate or to limit the extent of inflammatory tissue injury. This review discusses some of the basic concepts related to the immunoregulation of chronic gut inflammation and summarizes the current state of knowledge of the role that NO may play in modulating inflammatory tissue injury.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Humans
  • Immunity, Mucosal
  • Inflammation Mediators / physiology
  • Inflammatory Bowel Diseases / etiology*
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / physiopathology
  • Models, Biological
  • NF-kappa B / physiology
  • Nitric Oxide / physiology*
  • Nitric Oxide Synthase / physiology
  • Nitric Oxide Synthase Type II


  • Inflammation Mediators
  • NF-kappa B
  • Nitric Oxide
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II