Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases

Abstract

Inflammatory bowel disease (IBD) is a chronic disease in the gastrointestinal tract (GIT). IBD include ulcerative colitis (UC), which generally affects only the large intestine mucosa and submucosa, and Crohn’s disease (CD), which may affect any part of the GIT by transmural inflammation. Both UC and CD are associated with an imbalance of the gut microbiota composition and injuries in the intestinal mucosa. The intestinal dysbiosis is related to a reduction in butyrate-producing species, impairing the anti-inflammatory response of the immune system, and is commonly associated with micronutrients deficiency, e.g. vitamin D hypovitaminosis. Vitamin D is involved in several critical functions, including immune cell differentiation, regulation of microbiota, gene transcription, and barrier integrity. Vitamin D supplementation in IBD patients showed promising results in reducing the disease activity and modulating gut microbiota. Vitamin D receptor (VDR) regulates the biological actions of the active vitamin D metabolite, 1α,25-dihydroxyvitamin D3. Evidence supports that the VDR signaling is involved in the genetic, environmental, immune, and microbial aspects of IBD. Low VDR expression and dysfunction of vitamin D/VDR signaling are reported in IBD patients. Vitamin D/VDR deficiency could be considered as a multifunctional susceptibility factor in IBD. Therefore, in this review, we will discuss the progress in clinical studies, mechanism studies on Vitamin D /VDR, and potential use of vitamin D supplementation as adjuvant therapy to restore gut microbiota balance, promote beneficial metabolites, and inhibit inflammation status in patients with IBD.

Tryptophan Metabolites and Aryl Hydrocarbon Receptor in Severe Acute Respiratory Syndrome, Coronavirus-2 (SARS-CoV-2) Pathophysiology

“…Consequently, many of the effects of vitamin D on immune, mitochondria, epigenetic, and melatonergic pathway regulation may be mediated via effects in the gut. The prevention of gut permeability by vitamin D [ 53 ], may therefore be mediated via the upregulation of butyrate, whilst butyrate also acts to upregulate vitamin D receptor signaling [ 54 ]. Vitamin D may also suppress pro-inflammatory cytokine production [ 55 ], indicating that it may decrease pro-inflammatory cytokine-induced IDO, thereby impacting on the kynurenine/tryptophan ratio and inflammation driven AhR activation.…”

Distribution of intraepithelial lymphocytes, mast cells, and goblet cells in the intestine of alpaca

“…The goblet cells are scattered between the intestinal epithelial cells and resemble a high foot goblet, and their number gradually increases from the small to the large intestine, consistent with changes in intestinal bacteria (Battistini et al, 2020). The mucins secreted by goblet cells combine with extracellular water and inorganic salts to form a mucus layer, which interacts with intestinal epithelial cells, intestinal microecology, and the host's immune system to jointly maintain the homeostasis of the intestinal internal environment (Birchenough et al, 2015).…”

Alteration of gut microbiota during narrowband ultraviolet B therapy in psoriasis: A preliminary study

“…Vitamin D suppresses pro‐inflammatory responses 32 and enhances intestinal barrier integrity through regulation of the vitamin D receptor (VDR): VDR has been identified as the first human gene to shape the gut microbiome 33 . The gut dysbiosis‐associated inflammatory diseases, such as IBD and MS, are also strongly associated with vitamin D levels 34,35 Moreover, Lactobacillus was decreased in VDR depletion or failure of active vitamin D production 36 . A previous study also reported that the shift in gut microbiome after NBUVB exposure was associated with increased vitamin D levels 8 .…”