Effect of vitamin D on mast cells

Vitamin D is an essential fat soluble vitamin that functions as a hormone. Its primary function is to promote intestinal absorption of calcium, magnesium, phosphate, iron and zinc. It also has a variety of anti-inflammatory and immunoregulatory effects. Deficiency of vitamin D3 has been linked previously to a number of inflammatory conditions, like asthma, diabetes mellitus, eczema and other atopic disorders.

A significant portion of vitamin D is produced in the skin when exposed to sunlight. The precursor 7-dehydrocholesterol in the skin is changed to form cholecalciferol, vitamin D3, when irradiated with UVB light. In the liver, cholecalciferol (vitamin D3) is metabolized to form 25-dihydroxyvitamin D3. In the kidney, it is further metabolized to 1,25-dihydroxyvitamin D3. Vitamin D2 and D3 supplements may also be taken orally.  They will be processed by the liver in a similar fashion. Vitamin D3 is much more active than vitamin D2.

Vitamin D3 can exert a number of effects on mast cells. Though the mechanism is unclear, vitamin D3 seems to regulate the action of COX, the enzyme that produces prostaglandins.  Accordingly, vitamin D3 can disrupt prostaglandin production.

It interferes with the production of cytokines, and chemokines, including Il-1, IL-6, IL-33, and TNF. It inhibits release of IL-6 and CRP.  It is thought that vitamin D affects the stability of the mRNA for these molecules.  This means that the genes for these molecules are not being used appropriately and so they cannot be made.

Vitamin D3 can also induce production of anti-inflammatory mediators. IL-4 and IL-10 are mast cell mediators that regulate inflammation.  Vitamin D3 is required for their production and release.  IL-10 can mitigate inflammation resulting from IgE activation.  A single application of vitamin D3 to the skin decreased the immediate skin response to an IgE allergen.  It decreased production of leukotrienes and histamine.  Mast cells have vitamin D receptors (VDRs) inside their cells and close to where the genes are stored.  Mast cell VDRs must be present to see these effects.

Long term use of vitamin D3 (30-40 days) was found to cause mast cell apoptosis (programmed cell death) in a cell model. Vitamin D3 also directly impeded the differentiation and maturation of mast cell precursors.

There is a lot we do not know about how vitamin D3 interacts with mast cells but it is generally considered to have an anti-inflammatory and anti-allergic effect.

References:

Yip KH, et al. Mechanisms of vitamin D3 metabolite repression of IgE-dependent mast cell activation. Journal of Allergy and Clinical Immunology 2014: 13395), 1356-1364.e14

Conti P, Kempuraj D. Impact of vitamin D on mast cell activity, immunity and inflammation. Journal of Food and Nutrition Research 2016: 4(1), 33-39.

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