Vitamin D Regulation of Immune Function

Purpose of Review To review the mechanisms by which vitamin D and its metabolites regulate the immune system to facilitate the ability of the body to prevent and/or treat SARS-CoV2 and other respiratory infections and encourage further research into the role that vitamin D supplementation plays in preventing/treating such infections. Recent Findings Vitamin D deficiency is associated with an increased risk of SARS-CoV2 and other respiratory infections. Clinical trials in general demonstrate that correction of vitamin D deficiency reduces the risk of hospitalization, ICU admission, and death from SARS-CoV2 infection. The airway epithelium and alveolar macrophages express the enzyme, CYP27B1, that produces the active metabolite of vitamin D, 1,25(OH)(2)D, and the vitamin D receptor, VDR. Vitamin D and its metabolites promote the innate immune response, which provides the first line of defense against viral and bacterial infections while restricting the adaptive immune response, which if unchecked promotes the inflammatory response leading to the acute respiratory distress syndrome and death. The rationale for treating vitamin D deficiency to reduce the risk of SARS-CoV2 infection and supplementing patients with vitamin D early in the course of SARS-CoV2 infection rests primarily on the ability of vitamin D metabolites to promote an effective immune response to the infection.

Automated summary

This review examines the mechanisms by which vitamin D and its metabolites regulate the immune system to enhance the body's ability to prevent and/or treat SARS-CoV2 and other respiratory infections. Recent findings suggest that vitamin D deficiency is linked to an increased risk of such infections, while clinical trials show that correcting deficiency reduces the severity of SARS-CoV2 infection. Vitamin D and its metabolites promote innate immune response and restrict excessive inflammation, making them potential targets for prevention and treatment of respiratory infections.