Diet, gut microbes, and the pathogenesis of inflammatory bowel diseases. Issue 1 (15th August 2016)

• Record Type: Journal Article
• Authors: Dolan, Kyle T.; Chang, Eugene B.
• Other Names: Espin Juan Carlos guestEditor.
• Is Part Of: Molecular nutrition & food research. Volume 61:Issue 1(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2016-08-15
• Subjects: Diet -- IBD -- Microbial metabolism -- Microbiota -- Pathogenesis; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201600129
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Microbial metabolism of dietary compounds influences IBD pathophysiology. Key metabolites include short‐chain fatty acids (SCFA), which are used as fuel by epithelial cells and exert regulatory control via epigenetic mechanisms; bile acids and hydrogen sulfide (H2S), which initiate signaling pathways controlling intestinal permeability and inflammation and may be toxic at high concentrations; and AhR ligands such as indole‐3‐aldehyde, which promote defense against pathogens and differentiation of pro‐homeostatic Treg cells. Abstract : The rising incidence of inflammatory bowel diseases in recent decades has notably paralleled changing lifestyle habits in Western nations, which are now making their way into more traditional societies. Diet plays a key role in IBD pathogenesis, and there is a growing appreciation that the interaction between diet and microbes in a susceptible person contributes significantly to the onset of disease. In this review, we examine what is known about dietary and microbial factors that promote IBD. We summarize recent findings regarding the effects of diet in IBD epidemiology from prospective population cohort studies, as well as new insights into IBD‐associated dysbiosis. Microbial metabolism of dietary components can influence the epithelial barrier and the mucosal immune system, and understanding how these interactions generate or suppress inflammation will be a significant focus of IBD research. Our knowledge of dietary and microbial risk factors for IBD provides important considerations for developing therapeutic approaches through dietary modification or re‐shaping the microbiota. We conclude by calling for increased sophistication in designing studies on the role of diet and microbes in IBD pathogenesis and disease resolution in order to accelerate progress in response to the growing challenge posed by these complex disorders.