Vitamin D and host resistance to infection? Putting the cart in front of the horse

Abstract

Vitamin D is being touted as an anti-infective agent and it has even been suggested that vitamin D supplementation could be effective against the H1N1 influenza virus. The claims are largely based on the ability of vitamin D to induce antibacterial peptides and evidence that the immune system produces active vitamin D (1,25(OH)2D3) in situ. While there are many examples of immune production of 1,25(OH)2D3 in vitro, there is little in vivo evidence. In addition, it is not clear what role immune production of 1,25(OH)2D3 has on the course of disease. Vitamin D and 1,25(OH)2D3 inhibit T helper type 1 (Th1)/Th17-mediated immune responses and autoimmune diseases by acting on the innate and acquired immune system to inhibit the function of Th1 and Th17 cells. Th1 and Th17 cells are important in host resistance to many infections including tuberculosis (TB) caused by Mycobacterium tuberculosis. Paradoxically the innate immune system is induced to produce antibacterial peptides that are effective against TB in vitro. Data from several models of infection have so far not supported a role for vitamin D in affecting the course of disease. There is also very little evidence that vitamin D affects the course of human TB infection. Experiments have not been done in cells, mice or humans to evaluate the effect of vitamin D on influenza virus. At this time it would be premature to claim that vitamin D has an effect on TB, influenza or any other infection.