The role of microbial agents in the pathogenesis of inflammatory bowel disease

Inflammatory bowel disease (IBD) is a generic term that refers to Crohn's disease and ulcerative colitis. The precise aetiology of these diseases remains unknown. However, both are believed to result from the interaction of environmental factors, immune response and genetic factors. The impact...

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Bibliographic Details
Main Authors: Faujan, Nur Huda ,, Fatimah, Abu Bakar,, Shuhaimi, Mustafa,, Mohd Yazid, Abdul Manaf,, Loong Yik, Yee,
Format: Article
Language:en_US
Published: Lippincott Williams & Wilkins 2015
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Online Access:http://ddms.usim.edu.my/handle/123456789/8453
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Summary:Inflammatory bowel disease (IBD) is a generic term that refers to Crohn's disease and ulcerative colitis. The precise aetiology of these diseases remains unknown. However, both are believed to result from the interaction of environmental factors, immune response and genetic factors. The impact of environmental factors such as smoking, diet, drug, geographical and social status, stress, microbial agents, intestinal permeability and appendectomy appear to be associated with IBD pathogenesis. Some varieties of these factors modify gene expression in susceptible individuals and modulate the effector function of the intestinal immune system. To understand the IBD pathogenesis, several studies have reported that luminal bacteria play an essential role in development of IBDs. Various bacterial pathogens have been incriminated but the results obtained have been conflicting. No specific pathogen has been identified as being causally associated with IBD. However, it is widely thought that, in IBD cases, individuals appear to lose the normal tolerance to commensal bacteria leading to an elevated inflammatory response. By contrast to healthy gut, the symbiotic relationship between the host and the commensal bacteria exposure leads to the down-regulation of inflammatory genes. Therefore, this brief review focuses on the microbial aetiology of IBD. (c) 2007 Wolters Kluwer Health.