Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Disease
Read full article HERE
Department of Biology, University of British Columbia Okanagan, Kelowna, BC V1V 1V7, Canada;
The gastrointestinal (GI) microbiota is the collection of microbes which reside in the GI tract and represents the largest source of non-self antigens in the human body. The GI tract functions as a major immunological organ as it must maintain tolerance to commensal and dietary antigens while remaining responsive to pathogenic stimuli. If this balance is disrupted, inappropriate inflammatory processes can result, leading to host cell damage and/or autoimmunity. Evidence suggests that the composition of the intestinal microbiota can influence susceptibility to chronic disease of the intestinal tract including ulcerative colitis, Crohn’s disease, celiac disease and irritable bowel syndrome, as well as more systemic diseases such as obesity, type 1 diabetes and type 2 diabetes. Interestingly, a considerable shift in diet has coincided with increased incidence of many of these inflammatory diseases. It was originally believed that the composition of the intestinal microbiota was relatively stable from early childhood; however, recent evidence suggests that diet can cause dysbiosis, an alteration in the composition of the microbiota, which could lead to aberrant immune responses. The role of the microbiota and the potential for diet-induced dysbiosis in inflammatory conditions of the GI tract and systemic diseases will be discussed.
Microbial changes in the GI tract have profound effects on host inflammatory and metabolic responses. For example, protein-rich diets increase the activity of bacterial enzymes such as β-glucuronidase, azoreductase and nitroreductase, which produce toxic metabolites that trigger inflammatory responses. Because of the intricate balance that exists within the microbiota, alterations in one group or species may not only affect the host directly, but can also disrupt the entire microbial community. For example, members from the phyla Firmicutes, Actinobacteria, Verrucomicrobium and Bacteroidetes can degrade complex carbohydrates not absorbed by the host and can also inhibit the growth of opportunistic pathogens such as Clostridium spp. and members of Enterobacteriaceae like E. coli . Dysbiosis can also alter the metabolic activity of other members of the microbiota in the gut. Thus, it is conceivable that some diets promote the growth of microbes that could have detrimental effects on their host while other dietary factors could promote beneficial microbes. It is unknown whether diet-induced dysbiosis is a transient or long-term event. If dysbiosis is a long-term event, then postnatal nutrition could be used to promote changes in the microbiota early in life during the development of a more stable microbiota. In support of this, consumption of formula supplemented with fish oil has the capacity to alter the microbial composition in the infant; however, it is unknown if these microbial changes would be long lasting or transient. Although this study did not identify the specific microbes that changed, nor did it examine the effect on intestinal immunity, it does suggest that the microbiota could be modified through dietary factors to enrich beneficial microbes and prevent diseases associated with dysbiosis.