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Canadian Journal of Gastroenterology
Volume 26, Issue 9, Pages 631-637

The Impact of Farnesoid X Receptor Activation on Intestinal Permeability in Inflammatory Bowel Disease

Maja Stojancevic,1 Karmen Stankov,2 and Momir Mikov1

1Department of Pharmacology, Medical Faculty Novi Sad, University of Novi Sad, Hajduk Veljkova, Serbia
2Clinical Center of Vojvodina, Medical Faculty Novi Sad, University of Novi Sad, Hajduk Veljkova, Serbia

Received 25 July 2011; Accepted 30 December 2011

Copyright © 2012 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The most important function of the intestinal mucosa is to form a barrier that separates luminal contents from the intestine. Defects in the intestinal epithelial barrier have been observed in several intestinal disorders such as inflammatory bowel disease (IBD). Recent studies have identified a number of factors that contribute to development of IBD including environmental triggers, genetic factors, immunoregulatory defects and microbial exposure. The current review focuses on the influence of the farnesoid X receptor (FXR) on the inhibition of intestinal inflammation in patients with IBD. The development and investigation of FXR agonists provide strong support for the regulatory role of FXR in mucosal innate immunity. Activation of FXR in the intestinal tract decreases the production of proinflammatory cytokines such as interleukin (IL) 1-beta, IL-2, IL-6, tumour necrosis factor-alpha and interferon-gamma, thus contributing to a reduction in inflammation and epithelial permeability. In addition, intestinal FXR activation induces the transcription of multiple genes involved in enteroprotection and the prevention of bacterial translocation in the intestinal tract. These data suggest that FXR agonists are potential candidates for exploration as a novel therapeutic strategy for IBD in humans.