Abstract
Crohn’s Disease (CD) and Ulcerative Colitis (UC) are world-wide health problems in which intestinal dysbiosis or adverse functional changes in the microbiome are causative or exacerbating factors. The reduced abundance and diversity of the microbiome may be a result of a lack of exposure to vital commensal microbes or overexposure to competitive pathobionts during early life. Alternatively, many commensal bacteria may not find a suitable intestinal niche or fail to proliferate or function in a protective/competitive manner if they do colonize. Bacteria express a range of factors, such as fimbriae, flagella, and secretory compounds that enable them to attach to the gut, modulate metabolism, and outcompete other species. However, the host also releases factors, such as secretory IgA, antimicrobial factors, hormones, and mucins, which can prevent or regulate bacterial interactions with the gut or disable the bacterium. The delicate balance between these competing host and bacteria factors dictates whether a bacterium can colonize, proliferate or function in the intestine. Impaired functioning of NOD2 in Paneth cells and disrupted colonic mucus production are exacerbating features of CD and UC, respectively, that contribute to dysbiosis. This review evaluates the roles of these and other the host, bacterial and environmental factors in inflammatory bowel diseases.
Highlights
Crohn’s Disease (CD) and Ulcerative Colitis (UC) are global health problems
The present review looks at the role of these interactions and environmental factors in inflammatory bowel diseases (IBD) (Table 1)
This was evident in experimental studies in mice in which inflammation and colitis increased colonic epithelial oxygenation and facilitated a major expansion in aerobes, in particular Escherichia coli, like that often observed in IBD [178]
Summary
Crohn’s Disease (CD) and Ulcerative Colitis (UC) are global health problems. Previously considered to be mainly disorders of the developed world, the incidence of these inflammatory bowel diseases (IBD) is quickly increasing in the developing regions, in areas of rapid urbanization and industrialization [1,2,3]. Early- (6–10 years), very-early- (2–6 years) and infant- (under two years old) onset forms of IBD are often severe, even at first presentation. In this case, boys have a higher incidence of CD [4,5,6]. Predisposition to IBD has been linked to more than 200 gene susceptibility loci, including up to 50 of importance in very-early-onset IBD [10,11] These loci are associated with an array of metabolic systems, immune development and reactivity, epithelial cell function, gut barrier integrity, and interactions with and control of microbes.
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