Recent understanding of IBD pathogenesis: implications for future therapies

Inflamm Bowel Dis. 2006 Nov;12(11):1068-83. doi: 10.1097/01.mib.0000235827.21778.d5.


The inflammatory bowel diseases (IBD) are comprised of two major phenotypes, Crohn's disease (CD) and ulcerative colitis (UC). Research over the last couple of years has led to great advances in understanding the inflammatory bowel diseases and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses to a subset of luminal bacteria. Susceptibility to disease is thereby determined by genes encoding immune responses which are triggered by environmental stimuli. Based on extensive research over the last decade, there are several new and novel pathways and specific targets on which to focus new therapeutics. The following review summarizes the current view on the four basic tenets of the pathophysiological basis of IBD and its implications for therapies of IBD: genetics, immune dysregulation, barrier dysfunction and the role of the microbial flora.

Publication types

  • Review

MeSH terms

  • Bacterial Infections / complications*
  • Colitis, Ulcerative / etiology
  • Colitis, Ulcerative / genetics
  • Colitis, Ulcerative / immunology
  • Colitis, Ulcerative / therapy
  • Colon / microbiology
  • Colon / pathology
  • Crohn Disease / etiology
  • Crohn Disease / genetics
  • Crohn Disease / immunology
  • Crohn Disease / therapy
  • Genetic Predisposition to Disease
  • Humans
  • Inflammation Mediators / physiology
  • Inflammatory Bowel Diseases / etiology*
  • Inflammatory Bowel Diseases / genetics
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / therapy
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / physiopathology
  • Risk Factors


  • Inflammation Mediators