Role of vitamin D on gut microbiota in cystic fibrosis

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.

Keywords: Cystic fibrosis; Inflammation; Intestinal microbiota; Vitamin D; Vitamin D receptor.

Figure 1. A schematic representation of mechanisms by which vitamin D may decrease intestinal mucosal inflammation and thus alter dysbiosis in CF

Description: Microbial dysbiosis is a hallmark of the CF gut underlying to chronic mucosal inflammation. Vitamin D has been proposed to decrease intestinal inflammation through the inhibition of inflammation-induced epithelial cell apoptosis and enhancement of intercellular junctions that are important in maintaining mucosal permeability. In addition it reduces cytokine-induced NF-κB nuclear translocation thus resulting in a suppression of inflammatory mediators. Together, these effects may restore gastrointestinal homeostasis and prevent intestinal dysbiosis in CF.