Intestinal barrier dysfunction in inflammatory bowel diseases

Citations Over TimeTop 1% of 2008 papers

Abstract

The etiology of human inflammatory bowel diseases (IBDs) is believed to involve inappropriate host responses to the complex commensal microbial flora in the gut, although an altered commensal flora is not completely excluded. A multifunctional cellular and secreted barrier separates the microbial flora from host tissues. Altered function of this barrier remains a major largely unexplored pathway to IBD. Although there is evidence of barrier dysfunction in IBD, it remains unclear whether this is a primary contributor to disease or a consequence of mucosal inflammation. Recent evidence from animal models demonstrating that genetic defects restricted to the epithelium can initiate intestinal inflammation in the presence of normal underlying immunity has refocused attention on epithelial dysfunction in IBD. We review the components of the secreted and cellular barrier, their regulation, including interactions with underlying innate and adaptive immunity, evidence from animal models of the barrier's role in preventing intestinal inflammation, and evidence of barrier dysfunction in both Crohn's disease and ulcerative colitis.

Related Papers

• THE EXPERIMENTAL STUDY OF THE RELATED CYTOKINES FOR IN PATIENTS WITH ULCERATIVE COLITIS.(2005)
• Imbalance of intestinal flora induced by antibacterials,and its treatment and prevention(2009)
• Investigation of Serum NO Levels in Patients With Ulcerative Colitis(2002)
• Determination of plasma P-selection in patients with ulcerative colitis and their clinical significance(2004)
• The severity correlation of TNF-α,IL-6 and IL-8 levels in plasma in patients with ulcerative colitis and their clinical significances(2008)