Vitamin D influenza immunology vitamin d metabolism immune response
Abstract:
It has long been speculated that vitamin D plays an immunological role in the response to influenza infection. Previous studies by the Cantorna lab have shown that vitamin D deficiency or inability to produce 1,25(OH)2D, the active metabolite of vitamin D, throughout H1N1 influenza infection in mice resulted in increased lung inflammation and respiratory distress, as well as worse survival outcomes. To further understand the role of vitamin D in the H1N1 immune response, we investigated the expression levels of vitamin D metabolism and response genes, Cyp24a1, Cyp27b1, and the vitamin D receptor (Vdr) in mice that were vitamin D sufficient (D+) or deficient (D-), and in wildtype (WT) or knockout (KO) for Cyp27b1 mice. Cyp24a1 expression in the kidneys revealed that D+ WT mice exhibited the greatest vitamin D metabolism, especially post-infection. Lung experiments revealed that Cyp24a1 expression peaked with immune response at day 6, although neither Cyp27b1 nor Vdr expression followed a similar trend. Together, this data indicates that H1N1 infection may increase vitamin D metabolism, and future experiments will include investigating H1N1 M gene and proinflammatory cytokine expression to elicit a greater understanding of the role of vitamin D in the immune response and clearing the infection.
