Prebiotics, probiotics and helminths: the 'natural' solution?
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.


METHODS
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.
Guarner
Francisco
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
D000818:Animals; D006376:Helminths / Q000502:physiology*; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000382:microbiology / Q000469:parasitology; D007422:Intestines / Q000382:microbiology / Q000473:pathology; D054892:Metagenome / Q000502:physiology; D056692:Prebiotics; D019936:Probiotics / Q000627:therapeutic use*
D056692:Prebiotics