Diet-induced dysbiosis of the intestinal microbiota and the effects on immunity and disease

Abstract

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.

Keywords: disease susceptibility; inflammation; intestinal microbiota; nutrition.

Figure 1

Diet-induced dysbiosis affects disease susceptibility. The intestinal microbiome (microbial ecology and their genetic material) is influenced by both host genetics and the environment including dietary factors. In diseases including IBD, diabetes and obesity, diet is implicated as a contributing factor by having direct effects on host metabolism and/or immune responses. However, recent evidence suggests that diet also influences the composition of the microbiome. This could, in turn, affect host immunity and metabolism and alter susceptibility to disease.