201
Views
0
CrossRef citations to date
0
Altmetric
Review

Molecular Pathogenesis of Inflammatory Bowel Disease: Relevance for Novel Therapies

, &
Pages 609-626 | Published online: 10 Nov 2008
 

Abstract

The immense load of microorganisms within the gastrointestinal tract is a great challenge for the mucosal immune system. Whereas the vast majority of commensal bacteria should be tolerated, pathogenic organisms have to be attacked. During inflammatory bowel disease, the balanced interaction between the mucosal flora and the intestinal immune system is disturbed. Various defective components of this complex interaction have been described, such as different susceptibility genes, impaired innate immune responses and environmental factors, suggesting that inflammatory bowel diseases are multifactorial diseases. Based on new insights into the pathogenesis of inflammatory bowel disease, various targets for future drugs have been identified and new substances are emerging. The following article will review the current understanding of inflammatory bowel disease pathogenesis in context with genetic risk factors, imbalanced innate and acquired immune responses, and altered barrier function. Clinical treatment of the diseases will be summarized and emerging therapies as well as individual management based on recent insights into pathogenesis will be discussed.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.