Role of vitamin D on gut microbiota in cystic fibrosis

• Type of Material: Article
• Authors: Mansi Kanhere, Emory University; Benoit Chassaing, Georgia State University; Andrew Gewirtz, Emory University; Vin Tangpricha, Emory University
• Language: English
• Date: 2018-01-01
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2016 Elsevier Ltd
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.jsbmb.2016.11.001
• Title of Journal or Parent Work: Journal of Steroid Biochemistry and Molecular Biology
• ISSN: 0960-0760
• Volume: 175
• Start Page: 82
• End Page: 87
• Grant/Funding Information: Supported by a grant from the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR000454 (VT).
• Keywords: Life Sciences & Biomedicine; CUTTING EDGE; D DEFICIENCY; INTESTINAL EPITHELIAL-CELLS; Biochemistry & Molecular Biology; Endocrinology & Metabolism; Cystic fibrosis; METABOLIC SYNDROME; Vitamin D receptor; Inflammation; HEALTH; D-RECEPTOR; COLITIS; Vitamin D; FECAL MICROBIOTA; Intestinal microbiota; DISEASE; Science & Technology; PULMONARY EXACERBATIONS
• Research Categories: Biology, Molecular; Chemistry, Biochemistry; Health Sciences, Nutrition

Abstract

This review explores the potential for vitamin D to favorably alter the gut microbiota, given emerging evidence of the role of vitamin D in controlling mucosal inflammation in the gut. It will focus on cystic fibrosis (CF) patients, a population with both vitamin D deficiency due to gut malabsorption and an altered gut microbiota composition. Recent evidence shows that vitamin D acts to maintain the integrity of the gut mucosal barrier by enhancement of intercellular junctions that control mucosal permeability and reduction of pro-inflammatory cytokines such as IL-8. In addition, vitamin D receptor-mediated signaling has been shown to inhibit inflammation-induced apoptosis of intestinal epithelial cells. As a result of these effects on the intestinal mucosa, maintenance of sufficient vitamin D status may be essential for the development of a healthy gut microbiota, particularly in conditions defined by chronic mucosal inflammation such as CF. We hypothesize here that high dose vitamin D may be used to favorably manipulate the aberrant mucosa seen in patients with CF. This may result in improved clinical outcomes in association with a low inflammatory environment that allows beneficial bacteria to outcompete opportunistic pathogens. Current evidence is sparse but encouraging, and additional evidence is needed to establish vitamin D as a therapeutic approach for gut microbiota modification.