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World J Gastroenterol. Aug 14, 2006; 12(30): 4807-4812
Published online Aug 14, 2006. doi: 10.3748/wjg.v12.i30.4807
Etiopathogenesis of inflammatory bowel diseases
Silvio Danese, Claudio Fiocchi
Silvio Danese, Division of Gastroenterology, Istituto Clinico Humanitas-IRCCS in Gastroenterology, Milan, Italy
Claudio Fiocchi, Department of Pathobiology and Department of Gastroenterology and Hepatology, the Cleveland Clinic Foundation, Cleveland, Ohio, United States
Author contributions: All authors contributed equally to the work.
Supported by A grant from the Broad Medical Research Program to S.D
Correspondence to: Claudio Fiocchi, The Cleveland Clinic Foundation, Lerner Research Institute, Department of Pathobiology, 9500 Euclid Avenue, Cleveland, Ohio 44195, United States. fiocchc@ccf.org
Telephone: +1-216-4450895
Received: February 17, 2006
Revised: March 1, 2006
Accepted: March 10, 2006
Published online: August 14, 2006
Abstract

Theories explaining the etiopathogenesis of inflammatory bowel disease (IBD) have been proposed ever since Crohn’s disease (CD) and ulcerative colitis (UC) were recognized as the two major forms of the disease. Although the exact cause(s) and mechanisms of tissue damage in CD and UC have yet to be completely understood, enough progress has occurred to accept the following hypothesis as valid: IBD is an inappropriate immune response that occurs in genetically susceptible individuals as the result of a complex interaction among environmental factors, microbial factors, and the intestinal immune system. Among an almost endless list of environmental factors, smoking has been identified as a risk factor for CD and a protective factor for UC. Among microbial factors, no convincing evidence indicates that classical infectious agents cause IBD, while mounting evidence points to an abnormal immune response against the normal enteric flora as being of central importance. Gut inflammation is mediated by cells of the innate as well as adaptive immune systems, with the additional contribution of non-immune cells, such as epithelial, mesenchymal and endothelial cells, and platelets.

Keywords: Inflammatory bowel disease; Chronic inflammation; Mucosal immunity; Innate immunity; Adaptive immunity; Environment; Commensal flora