COMMENTARY

Inflammatory bowel disease

Inflammatory bowel disease: is it really just another break in the wall?

C R Weber, J R Turner

Department of Pathology, University of Chicago, Chicago, Illinois, USA

Correspondence to:
Correspondence to:
Dr J R Turner
University of Chicago, 5841 South Maryland, MC 1089, Chicago, IL 60637, USA; jturner@bsd.uchicago.edu

---

Although the critical factors necessary for IBD pathogenesis remain mysterious, interest in the potential role of defective epithelial barrier function continues to grow. New insight into the mechanisms responsible for barrier dysfunction in IBD may lead to understanding its contribution to disease development and progression.

---

The first 150 words of the full text of this article appear below.

Ulcerative colitis and Crohn’s disease, collectively known as inflammatory bowel disease (IBD), are major causes of lifetime morbidity. Although these diseases are often differentiated clinically on the basis of disease distribution and morphology, they share many characteristics. Each disease clearly involves an abnormal mucosal inflammatory response, and data from various sources suggest that luminal stimuli and epithelial cell dysfunction can also contribute to disease pathogenesis or progression. Defective epithelial barrier function, which can be measured as increased intestinal permeability, has been implicated in IBD¹ and can predict relapse during clinical remission.^2,3 Increased permeability is also present in a subset of unaffected first-degree relatives of patients with Crohn’s disease.^4,5 As a result of these observations, the mechanisms of barrier function and permeability defects are thought to have a great potential in defining IBD pathogenesis and guiding the development of novel treatments.

The mucosal barrier is established by the . . . [Full text of this article]

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

Relevant Article

Changes in expression and distribution of claudin 2, 5 and 8 lead to discontinuous tight junctions and barrier dysfunction in active Crohn’s disease

S Zeissig, N Bürgel, D Günzel, J Richter, J Mankertz, U Wahnschaffe, A J Kroesen, M Zeitz, M Fromm, and J-D Schulzke
Gut 2007 56: 61-72. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

• Muise, A M, Walters, T D, Glowacka, W K, Griffiths, A M, Ngan, B-Y, Lan, H, Xu, W, Silverberg, M S, Rotin, D (2009). Polymorphisms in E-cadherin (CDH1) result in a mis-localised cytoplasmic protein that is associated with Crohn's disease. Gut 58: 1121-1127 [Abstract] [Full Text]  
• Vojdani, A., Lambert, J. (2009). The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II. Evid Based Complement Alternat Med 0: nep063v1-nep063 [Abstract] [Full Text]  
• Dabek, M., Ferrier, L., Roka, R., Gecse, K., Annahazi, A., Moreau, J., Escourrou, J., Cartier, C., Chaumaz, G., Leveque, M., Ait-Belgnaoui, A., Wittmann, T., Theodorou, V., Bueno, L. (2009). Luminal Cathepsin G and Protease-Activated Receptor 4: A Duet Involved in Alterations of the Colonic Epithelial Barrier in Ulcerative Colitis. Am. J. Pathol. 175: 207-214 [Abstract] [Full Text]  
• Clarke, L. L. (2009). A guide to Ussing chamber studies of mouse intestine. Am. J. Physiol. Gastrointest. Liver Physiol. 296: G1151-G1166 [Abstract] [Full Text]  
• Fasano, A. (2008). Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation: Living Life on the Edge of the Wall. Am. J. Pathol. 173: 1243-1252 [Abstract] [Full Text]  
• Gecse, K, Roka, R, Ferrier, L, Leveque, M, Eutamene, H, Cartier, C, Ait-Belgnaoui, A, Rosztoczy, A, Izbeki, F, Fioramonti, J, Wittmann, T, Bueno, L (2008). Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic lumenal factor impairing colonic permeability and sensitivity. Gut 57: 591-599 [Abstract] [Full Text]  
• Al-Sadi, R., Ye, D., Dokladny, K., Ma, T. Y. (2008). Mechanism of IL-1{beta}-Induced Increase in Intestinal Epithelial Tight Junction Permeability. J. Immunol. 180: 5653-5661 [Abstract] [Full Text]