Published online Mar 21, 2016. doi: 10.3748/wjg.v22.i11.3117
Peer-review started: June 21, 2015
First decision: August 26, 2015
Revised: September 19, 2015
Accepted: December 19, 2015
Article in press: December 19, 2015
Published online: March 21, 2016
Inflammatory bowel diseases are characterised by inflammation that compromises the integrity of the epithelial barrier. The intestinal epithelium is not only a static barrier but has evolved complex mechanisms to control and regulate bacterial interactions with the mucosal surface. Apical tight junction proteins are critical in the maintenance of epithelial barrier function and control of paracellular permeability. The characterisation of alterations in tight junction proteins as key players in epithelial barrier function in inflammatory bowel diseases is rapidly enhancing our understanding of critical mechanisms in disease pathogenesis as well as novel therapeutic opportunities. Here we give an overview of recent literature focusing on the role of tight junction proteins, in particular claudins, in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer.
Core tip: Epithelial barrier function is compromised in inflammatory bowel diseases (IBD). Apical tight junction proteins, in particular claudins, are key players in epithelial barrier function. However, there is little consensus regarding the expression of most claudin isoforms in these conditions or whether these findings are primary or secondary to disease pathogenesis. Knowledge of tight junction protein expression and function in IBD and IBD associated colorectal cancer will enhance our understanding of critical mechanisms in disease pathogenesis as well as novel therapeutic opportunities.