Int J Med Microbiol. 2009 Sep 30.
Inflammatory bowel disease, gut bacteria and probiotic therapy.
Reiff C, Kelly D.
Department of Gut Immunology, Rowett Institute of Nutrition and Health, Greenburn Road, Bucksburn, AB21 9SB Aberdeen, UK.
Crohn's disease (CD) and ulcerative colitis (UC) are the two major forms of inflammatory bowel disease (IBD) and both diseases lead to high morbidity and health care costs. Complex interactions between the immune system, enteric commensal bacteria and host genotype are thought to underlie the development of IBD although the precise aetiology of this group of diseases is still unknown. The understanding of the composition and complexity of the normal gut microbiota has been greatly aided by the use of molecular methods and is likely to be further increased with the advent of metagenomics and metatranscriptomics approaches, which will allow an increasingly more holistic assessment of the microbiome with respect to both diversity and function of the commensal gut microbiota. Studies thus far have shown that the intestinal microbiota drives the development of the gut immune system and can induce immune homeostasis as well as contribute to the development of IBD.
Probiotics which deliver some of the beneficial immunomodulatory effects of the commensal gut microbiota and induce immune homeostasis have been proposed as a suitable treatment for mild to moderate IBD. This review provides an overview over the current understanding of the commensal gut microbiota, its interactions with the mucosal immune system and its capacity to induce both gut homeostasis as well as dysregulation of the immune system. Bacterial-host events, including interactions with pattern recognition receptors (PRRs) expressed on epithelial cells and dendritic cells (DCs) and the resultant impact on immune responses at mucosal surfaces will be discussed.
PMID: 19800289
Dig Dis. 2009;27(3):412-7. Epub 2009 Sep 24.
Prebiotics, probiotics and helminths: the 'natural' solution?
Guarner F.
Digestive System Research Unit, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), University Hospital Vall d'Hebron, ES-08035 Barcelona, Spain. fguarner@vhebron.net
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-beta 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. Copyright 2009 S. Karger AG, Basel.
PMID: 19786773 
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