Introduction
Vitamin D is both a vitamin obtained through the diet and a hormone produced by our bodies. It is a fat-soluble vitamin that aids in the absorption and retention of calcium and phosphorus, both of which are essential for bone formation. Vitamin D has also been shown in laboratory studies to inhibit cancer cell development, aid infection control, and reduce inflammation. Vitamin D receptors can be found in a variety of organs and tissues throughout the body, suggesting that it has vital functions beyond bone maintenance.
Vitamin D is only found in a few foods naturally, but it is fortified in others. Because it is difficult to eat enough vitamin D from food, the best option for most individuals to acquire enough is to take a supplement. Vitamin D supplements come in two types: vitamin D2 (also known as ergocalciferol or pre-vitamin D) and vitamin D3 (sometimes known as cholecalciferol). Both are naturally occurring forms that are produced in the presence of ultraviolet-B (UVB) rays from the sun, earning it the nickname "the sunshine vitamin," but D2 is produced by plants and fungi, while D3 is produced by animals, including humans. Vitamin D is produced primarily in the skin, but many people have insufficient amounts because they live in areas where sunshine is limited in the winter or because they have little sun exposure due to spending most of their time indoors. Also, those with darker skin have lower vitamin D blood levels because the pigment melanin serves as a shade, limiting vitamin D production. This also reduces the damaging effects of sunlight on the skin and reduces the risk of skin cancer.
Although vitamin D is best known for its role in calcium homeostasis, it also has a number of direct and indirect immune-system regulatory effects, including promoting regulatory T cells (Tregs), inhibiting Th1 and Th17 cell differentiation, impairing B cell development and function, and lowering monocyte activation. Vitamin D may have medicinal potential due to its immunosuppressive properties. In reality, several preclinical investigations in MS (multiple sclerosis) and colitis models (though fewer in arthritis and lupus) have shown that oral or intraperitoneal vitamin D treatment is beneficial. However, clinical investigations have failed to show a clear advantage, implying that the relationship between vitamin D and autoimmunity is more complex than previously thought.
What Is the Gut Microbiome?
The human microbiome is defined as an ecological community of commensal, symbiotic, and pathogenic microbes that live on and in our bodies. It is made up of 12 different bacterial phyla, with Bacteroidetes, Proteobacteria, Firmicutes, Actinobacteria, and Euryarchaeota accounting for 93.5 percent of the total. Intestinal microorganisms aid in the breakdown of food into chemicals and nutrients that the body can absorb and consume. The gut microbiome has been shown to have an essential role in molding the immune system and contributing to health and disease in the last ten years. Due to molecular mimicry, the hypothesis that foreign microbial peptides may exhibit structure and sequence characteristics with self-antigens and hence be capable of activating immune cell auto-reactivity, the microbiome is of special interest in autoimmunity.
The Gut Microbiota and Vitamin D:
A proper balance of micronutrients, vitamins, and minerals, including vitamin D, is essential for good health and disease control. Infantile rickets and adult osteomalacia are caused by vitamin D deficiency. Low vitamin D levels have been linked to an increased risk of hypertension, diabetes, peripheral artery disease, cardiovascular disease, certain cancers, and autoimmune and inflammatory diseases. Vitamin D deficiency is common, especially in areas with little sunlight exposure, and may impair normal intestinal homeostasis and barrier functions by influencing the tight junction architecture, bacterial colonization, and anti-inflammatory responses.
What Effect Does Vitamin D Deficiency Have on Intestinal Bacteria and Autoimmunity?
Vitamin D deficiency has shown an association with autoimmune illness by affecting the microbiota and immune system.
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Vitamin D shortage or supplementation alters the microbiome, and changing the number or makeup of bacteria has an impact on disease manifestation.
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Physical and functional barrier integrity can be compromised by a lack of vitamin D signaling caused by a dietary shortage or a genetic defect in VDR expression or activity. This allows germs to interact with the host, causing immunological responses to be stimulated or inhibited.
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In the case of vitamin D insufficiency, our natural, intrinsic immune defenses may be weakened.
The Gut Microbiota Is Influenced by Vitamin D Supplementation:
Significant links have been discovered between vitamin D and the gut microbiota. During vitamin D supplementation, a shift in microbial composition was observed.
The Epithelial Barrier in the Gut Mucosa Is Protected by Vitamin D:
Vitamin D regulates gut mucosa homeostasis by maintaining the integrity of the epithelial barrier and healing the epithelium. Vitamin D protects the epithelial barrier by increasing the expression of VDR (vitamin D receptor) associated intercellular junction proteins, which form tight junctions between epithelial cells. Inadequate vitamin D levels increase the mucous membrane's susceptibility to damage, increasing the risk of inflammatory bowel disorder (IBD) significantly. Numerous studies have shown that patients with IBD frequently have vitamin D deficiency, even in remission. A low vitamin D level is an external risk factor for IBD exacerbation.
Bacteria Regulate VDR Expression in the Gut Microbiota and Their Fermentation Products:
Interactions between vitamin D and VDR help maintain gut homeostasis by preventing pathogen invasion, suppressing inflammation, and maintaining cell integrity. VDR expression and location may thus be regulated by both commensal and pathogenic gut microbiota. Probiotics can boost VDR expression and activity in the host, reducing intestinal inflammation.
Probiotic Bacteria Raise the Level of 25-Hydroxyvitamin D in the Blood:
Low levels of 25-hydroxyvitamin D in the blood have been linked to inflammatory bowel disease.
Conclusion
Vitamin D has anti-inflammatory and immune-modulating properties in the GIT (gastrointestinal tract). Many of these functions, which impact the human microbiome, occur as a result of complex ligand-receptor communication between vitamin D and VDR. Vitamin D is also involved in innate and adaptive immunity, intestinal barrier integrity, and gut homeostasis. Vitamin D regulates the gut microbiota because vitamin D deficiency causes a microbial imbalance in the GIT. Vitamin D's antibacterial effect is linked to the expression of antimicrobial peptides (AMPs). The gut microbiota responds to exogenous vitamin D, and some microbiota fermentation products can induce VDR expression.
