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

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.

The Potential of Vitamin D3 to Repaired Mucosal Injury in Dextran Sulfate Sodium Induced Acute Colitis in Mice

“…In agreement with the previous studies that stated VDR expressed in Lgr5 colon stem cells in human tissue in normal conditions [20]. Temporarily, Ki-67 indicate cell proliferation and differentiation marker and found significantly increased in the previous study compared to non-colitis mice [21]. While the analysis also identified the proliferation index Ki67 was found to slightly decreased in colonic epithelial crypts from damaged mucosa.…”

“…The lower serum Vitamin D 3 levels by colitis condition were in turn implicated in the rapid inactivation of VDR expression in Lgr5+ cells or Ki-67 and a subsequent loss of stem cell function. Therefore, low Vitamin D 3 exposure was considered similar to the stress induced by radiation and chemically induced inflammation, implicating Vitamin D 3 as an extrinsic variable that determines the function of Lgr5+ and Ki-67 in colon stem cells [17], [21], [22], [23]. However, there are limitations to knowing that IHC/IF does not have precise accuracy for counting proteins, and it would be better to use Western Blot or ELISA.…”

Vitamin D and Microbiota: Is There a Link with Allergies?

“…In humans, the major source of vitamin D (90%) is the exposure to solar UVB radiation, which determines the formation of cholecalciferol in the skin, which is then metabolized in the liver, by the vitamin D 25-hydroxylase Cyp2R1 and to a lesser extent by Cyp27A1, to 25-hydroxyvitamin D (25-OH-D3) and finally carried to the kidneys, where it is transformed into the active form (1,25-dihydroxyvitamin D, 1,25-(OH)2D) [ 3 ]. Only 10% of vitamin D is obtained through food ingestion (with vitamin D-rich foods such as cod liver oil, tuna, sardines, milk, eggs, certain mushrooms, and fortified orange juice and dairy products) [ 15 ].…”

Role of Vitamin D in Colorectal Cancer: A Holistic Approach and Review of the Clinical Utility

“…The accelerated growth of the tumor and malignancy were contributed to the hyperactive Wnt/β-catenin pathway after the loss of VDR. As compared to healthy colon cells, there was a notable increase in the colonic Wnt and β-catenin stained cells in colorectal and colitis patients, with an increase of 4.5 folds and 2.5 folds, respectively [ 16 ]. 1,25D suppresses β-catenin transcriptional activity.…”