Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review

Molecules. 2020 May 14;25(10):2300. doi: 10.3390/molecules25102300.

Abstract

Vitamin D is widely known to regulate bone health, but there is increasing evidence that it may also ameliorate colitis through inflammation, cell proliferation and apoptosis, and the microbiota. The purpose of this review is to systematically examine the mechanisms by which vitamin D reduces colitis. PubMed and Web of Science were searched for articles published between 2008 and 2019 using key words such as "vitamin D," "colitis," "inflammatory bowel disease," "inflammation," "apoptosis," "cell proliferation," and "gut bacteria". Retrieved articles were further narrowed and it was determined whether their title and abstracts contained terminology pertaining to vitamin D in relation to colitis in human clinical trials, animal studies, and cell culture/biopsy studies, as well as selecting the best match sorting option in relation to the research question. In total, 30 studies met the established criteria. Studies consistently reported results showing that vitamin D supplementation can downregulate inflammatory pathways of COX-2, TNF-α, NF-κB, and MAPK, modify cell kinetics, and alter gut microbiome, all of which contribute to an improved state of colitis. Although vitamin D and vitamin D analogs have demonstrated positive effects against colitis, more randomized, controlled human clinical trials are needed to determine the value of vitamin D as a therapeutic agent in the treatment of colitis.

Keywords: cell kinetics; gut microbiome; inflammation; inflammatory bowel disease; vitamin D.

Publication types

  • Review

MeSH terms

  • Animals
  • Clinical Trials as Topic
  • Colitis / diet therapy*
  • Colitis / genetics
  • Colitis / microbiology
  • Colitis / pathology
  • Colon / drug effects
  • Colon / microbiology
  • Colon / pathology
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Dietary Supplements*
  • Epithelial Cells / drug effects
  • Epithelial Cells / microbiology
  • Epithelial Cells / pathology
  • Gastrointestinal Microbiome / drug effects
  • Gastrointestinal Microbiome / physiology
  • Gene Expression Regulation / drug effects*
  • Humans
  • Inflammation
  • Inflammatory Bowel Diseases / diet therapy*
  • Inflammatory Bowel Diseases / genetics
  • Inflammatory Bowel Diseases / microbiology
  • Inflammatory Bowel Diseases / pathology
  • Mice
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Vitamin D / administration & dosage*

Substances

  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Vitamin D
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Mitogen-Activated Protein Kinases