Role of vitamin D on gut microbiota in cystic fibrosis.
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.
Division of Endocrinology, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Mansi
M
Kanhere
Center for Inflammation, Immunity, & Infection, Institute for Biomedical Sciences, Georgia State University, USA.
Benoit
B
Chassaing
Center for Inflammation, Immunity, & Infection, Institute for Biomedical Sciences, Georgia State University, USA.
Andrew T
AT
Gewirtz
Division of Endocrinology, Metabolism, and Lipids, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA; Atlanta VA Medical Center, Decatur, GA, USA. Electronic address: vin.tangpricha@emory.edu.
Vin
V
Tangpricha
D000818:Animals; D003550:Cystic Fibrosis / Q000150:complications / Q000178:diet therapy / Q000276:immunology / Q000378:metabolism*; D064806:Dysbiosis / Q000150:complications / Q000178:diet therapy / Q000276:immunology / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D000069196:Gastrointestinal Microbiome / Q000187:drug effects* / Q000276:immunology; D041981:Gastrointestinal Tract / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D007365:Intercellular Junctions / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000276:immunology; D007413:Intestinal Mucosa / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D051379:Mice; D018167:Receptors, Calcitriol / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction; D014807:Vitamin D / Q000008:administration & dosage / Q000276:immunology / Q000378:metabolism*; D014808:Vitamin D Deficiency / Q000150:complications / Q000178:diet therapy / Q000276:immunology / Q000378:metabolism*
D016209:Interleukin-8; D018167:Receptors, Calcitriol; C579457:VDR protein, human; D014807:Vitamin D
Cystic fibrosis; Inflammation; Intestinal microbiota; Vitamin D; Vitamin D receptor