[Inflammatory bowel disease: IBD]

Rinsho Byori. 2009 Jun;57(6):527-32.
[Article in Japanese]

Abstract

Inflammatory bowel diseases (IBD) are chronic, relapsing inflammatory disorders of the gastrointestinal tract, which are represented mainly by ulcerative colitis and Crohn's disease. Although the cause of IBD remains unknown, immunological abnormalities triggered by genetic and environmental factors are thought to be important in its pathogenesis. Recently, the intestinal microflora have been thought to be an important and essential environmental factor in their etiology. There are two major hypotheses which explain the relationship between the intestinal microflora and the pathogenesis of IBD. The first hypothesis is that IBD are caused by abnormal immunological responses to the normal intestinal microflora. In this case, disorders of the mucosal innate immune systems, such as functional disorders of NOD, lead to excessive immune responses and cause mucosal inflammation of the gut. The second hypothesis is that IBD are caused by fundamental, abnormal changes in the intestinal microflora. In this case, the changes in the composition of the intestinal microflora lead to pathogenic responses and cause mucosal inflammation of the gut. Recently, molecular approaches that facilitate evaluation of alterations in non-cultivatable intestinal bacteria in IBD patients have supported the latter hypothesis.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Animals
  • Humans
  • Immunity, Innate
  • Inflammatory Bowel Diseases* / etiology
  • Inflammatory Bowel Diseases* / immunology
  • Inflammatory Bowel Diseases* / microbiology
  • Intestines / microbiology
  • Mutation
  • Nod2 Signaling Adaptor Protein / genetics

Substances

  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein