Background: The pathophysiological mechanisms that generate chronic inflammatory lesions in inflammatory bowel disease (IBD) have, at least in part, been unveiled. Abnormal communication between gut microbial communities and the mucosal immune system is being incriminated as the core defect leading to intestinal injury in genetically susceptible individuals. The therapeutic manipulation of gut microecology has attracted high expectation as a strategic area for the control and prevention of IBD. Method: Literature review. Results: The gut is the major site for induction of regulatory T cells, which secrete immunoregulatory cytokines such as IL-10 and TGF-β and can regulate both Th1 and Th2 responses. Recent findings suggest that some gut commensals, including lactobacilli, bifidobacteria and helminths, play a major role in the induction of regulatory T cells in gut lymphoid follicles. Such T cell-mediated regulatory pathways are essential homeostatic mechanisms by which the host can tolerate the massive burden of innocuous antigens within the gut without responding through inflammation. In clinical practice, the evidence for the use of probiotics or prebiotics is strongest in the case of pouchitis. In addition, one probiotic strain appears to be equivalent to mesalazine in maintaining remission of ulcerative colitis. However, studies of probiotics in Crohn’s disease have been disappointing. Conclusions: Further research is needed to optimize the use of probiotics, prebiotics or helminths for these indications.
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