Abnormal intestinal permeability in Crohn's disease pathogenesis
Version of Record online: 25 JUN 2012
© 2012 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1258, Barriers and Channels Formed by Tight Junction Proteins II pages 159–165, July 2012
How to Cite
Teshima, C. W., Dieleman, L. A. and Meddings, J. B. (2012), Abnormal intestinal permeability in Crohn's disease pathogenesis. Annals of the New York Academy of Sciences, 1258: 159–165. doi: 10.1111/j.1749-6632.2012.06612.x
- Issue online: 25 JUN 2012
- Version of Record online: 25 JUN 2012
- Crohn's disease;
- experimental colitis;
- intestinal permeability;
Increased small intestinal permeability is a longstanding observation in both Crohn's disease patients and in their healthy, asymptomatic first-degree relatives. However, the significance of this compromised gut barrier function and its place in the pathogenesis of the disease remains poorly understood. The association between abnormal small intestinal permeability and a specific mutation in the NOD2 gene, which functions to modulate both innate and adaptive immune responses to intestinal bacteria, suggests a common, genetically determined pathway by which an abnormal gut barrier could result in chronic intestinal inflammation. Furthermore, rodent colitis models show that gut barrier defects precede the development of inflammatory changes. However, it remains possible that abnormal permeability is simply a consequence of mucosal inflammation. Further insight into whether abnormal barrier function is the cause or consequence of chronic intestinal inflammation will be crucial to understanding the role of intestinal permeability in the pathogenesis of Crohn's disease.