Premium
Inflammatory Bowel Disease and the Apical Junctional Complex
Author(s) -
BRUEWER MATTHIAS,
SAMARIN STANISLAV,
NUSRAT ASMA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1326.017
Subject(s) - proinflammatory cytokine , tight junction , adherens junction , barrier function , tumor necrosis factor alpha , cell junction , inflammatory bowel disease , microbiology and biotechnology , intestinal mucosa , chemistry , intestinal permeability , immunology , inflammation , biology , pathology , cadherin , medicine , disease , cell , biochemistry
A critical function of the intestinal mucosa is to form a barrier that separates luminal contents from the underlying interstitium. This intestinal barrier is primarily regulated by the apical junctional complex (AJC) consisting of tight junctions (TJs) and adherens junctions (AJs) and is compromised in a number of intestinal diseases, including inflammatory bowel disease (IBD). In vitro studies have demonstrated that proinflammatory cytokines, such as interferon‐gamma (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α), that are increased in the intestinal mucosa of patients with IBD can induce a leaky mucosal barrier. There is a growing evidence that the increased permeability and altered AJC structure observed in IBD are mediated by internalization of junctional proteins. This review summarizes barrier defects observed in IBD and addresses mechanisms by which proinflammatory cytokines, such as IFN‐γ and TNF‐α, modulate AJC structure and epithelial barrier function.