Research on Prebiotics and Digestive Disorders: Crohn’s, IBS, Ulcerative Colitis, etc.
Clinical, microbiological, and immunological effects of fructo-oligosaccharide in patients with Crohn's disease.
Lindsay JO et al; Gut. 2006; 55(3): P-348-55
- The intestinal microbiota play a pivotal role in the inflammation associated with Crohn's disease through their interaction with the mucosal immune system.
- Some bifidobacteria species are immunoregulatory and induce increased dendritic cell interleukin 10 (IL-10) release in vitro.
- Fructo-oligosaccharides (FOS) increase faecal and mucosal bifidobacteria in healthy volunteers.
- FOS supplementation increases faecal bifidobacteria concentrations and modifiesmucosal dendritic cell function.
- This novel therapeutic strategy appears to decrease Crohn's disease activity in a small open label trial and therefore warrants further investigation.
Evidence for the use of probiotics and prebiotics in inflammatory bowel disease: a review of clinical trials.
Hedin C et al; Proc Nutr Soc. 2007; 66(3): P-307-15
- Human subjects and their enteric microbiota have evolved together to reach a state of mutual tolerance. Mounting evidence from both animal models and human studies suggests that inflammatory bowel disease (IBD) represents a malfunction of this relationship.
- A range of probiotic, prebiotic and combination (synbiotic) treatments have been tested in a variety of patient groups with an assortment of end points.
- Conclusions about any one treatment in a specific patient group can therefore only be drawn on evidence from relatively small numbers of patients.
- The present article reviews the role of the intestinal microbiota in the pathogenesis of IBD and addresses the clinical evidence for the therapeutic manipulation of bowel microbiota using probiotics, prebiotics and synbiotics in IBD.
Inulin and oligofructose in chronic inflammatory bowel disease.
Leenen CH, Dieleman LA; J Nutr. 2007; 137(11 Suppl): P-2572S
- Crohn's disease and ulcerative colitis, also called chronic inflammatory bowel diseases (IBD), affect up to 500 per 100,000 persons in the Western world.
- Recent studies in the etiology of IBD suggest that these diseases are caused by a combination of genetic, environmental, and immunological factors.
- Results from humans and especially animal models of colitis reported by our group and others have indicated that these diseases result from a lack of tolerance to resident intestinal bacteria in genetically susceptible hosts.
- Prebiotics are nondigestible dietary oligosaccharides that affect the host by selectively stimulating growth, activity, or both of selective intestinal (probiotic) bacteria.
- Prebiotics are easy to administer and, in contrast to probiotic therapy, do not require administration of large amounts of (live) bacteria and are therefore easier to administer.
- Studies using prebiotics, especially beta-fructan oligosaccharides, for the treatment of chronic intestinal inflammation have shown benefit in animal models of colitis.
- These dietary therapies could lead to novel treatments for these chronic debilitating diseases.
Prebiotics in inflammatory bowel diseases.
Guarner F; Br J Nutr. 2007; 137(Suppl 1): P-S85-9
- Experimental and human studies have shown that inulin and oligofructose stimulate saccharolysis in the colonic lumen and favour the growth of indigenous lactobacilli and bifidobacteria.
- These effects are associated with reduced mucosal inflammation in animal models of IBD.
- Strong experimental evidence supports the hypothesis that inulin and oligofructose can offer an opportunity to prevent or mitigate intestinal inflammatory lesions in human Crohn's disease, ulcerative colitis, and pouchitis.
- Encouraging results have been obtained in preliminary clinical trials.
Probiotics and prebiotics in gastrointestinal disorders.
Fedorak RN, Madsen KL; Curr Opin Gastroenterol. 2004; 20(2): P-146-55
- This review summarizes the clinical efficacy of probiotics and prebiotics in gastrointestinal disorders and examines the mechanisms of action related to their therapeutic effect.
- The demonstration that immune and epithelial cells can discriminate between different microbial species has extended the known mechanism(s) of action of probiotics beyond simple barrier and antimicrobial effects. It has also confirmed that probiotic bacteria modulate mucosal and systemic immune activity and epithelial function.
- The progressive unraveling of these mechanisms of action has led to new credence for the use of probiotics and prebiotics in clinical medicine.
- The use of probiotics and prebiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into the "mainstream." Mechanisms of action explain the therapeutic effects and randomized; controlled trials provide the necessary evidence for their incorporation into the therapeutic armamentarium.
Prebiotics in chronic intestinal inflammation.
Looijer-van Langen MA, Dieleman LA. Centre of Excellence for Gastrointestinal Inflammation and Immunity Research, University of Alberta, Edmonton, Alberta, Canada.
- Older as well as more recent studies show beneficial effects of prebiotics in experimental colitis and lately also in human inflammatory bowel diseases (IBD), such as Crohn's disease, ulcerative colitis, and chronic pouchitis.
- In this review we give an overview of the benefits of prebiotics in rodent IBD models and in IBD patients and discuss their possible protective mechanisms.
- Commensal intestinal bacteria induce and perpetuate chronic intestinal inflammation, whereas others are protective. However, most of the current medications are directed against the exaggerated proinflammatory immune response of the host, some of them toxic and costly.
- Feeding prebiotics changes the composition of the intestinal microflora toward more protective intestinal bacteria and alters systemic and mucosal immune responses of the host.
- Prebiotics have the promise to be relatively safe, inexpensive, and easy to administer.
- Unraveling their protective mechanisms will help to develop rational applications of prebiotics.