Oral Supplementation of the Vitamin D Metabolite 25(OH)D3 Against Influenza Virus Infection in Mice

• Published in: Nutrients Vol. 12; no. 7; p. 2000
• Main Authors: Hayashi, Hirotaka, Okamatsu, Masatoshi, Ogasawara, Honami, Tsugawa, Naoko, Isoda, Norikazu, Matsuno, Keita, Sakoda, Yoshihiro
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 05.07.2020; MDPI
• Subjects: Chromatography; Cytokines; Diet; Infections; Influenza; Kidneys; Lungs; Lymphocytes; Small intestine; Tumor necrosis factor-TNF; Vitamin D; United States > US; Japan
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu12072000

Vitamin D is a fat-soluble vitamin that is metabolized by the liver into 25-hydroxyvitamin D [25(OH)D] and then by the kidney into 1,25-dihydroxyvitamin D [1,25(OH)2D], which activates the vitamin D receptor expressed in various cells, including immune cells, for an overall immunostimulatory effect. Here, to investigate whether oral supplementation of 25-hydroxyvitamin D3 [25(OH)D3], a major form of vitamin D metabolite 25(OH)D, has a prophylactic effect on influenza A virus infection, mice were fed a diet containing a high dose of 25(OH)D3 and were challenged with the influenza virus. In the lungs of 25(OH)D3-fed mice, the viral titers were significantly lower than in the lungs of standardly fed mice. Additionally, the proinflammatory cytokines IL-5 and IFN-γ were significantly downregulated after viral infection in 25(OH)D3-fed mice, while anti-inflammatory cytokines were not significantly upregulated. These results indicate that 25(OH)D3 suppresses the production of inflammatory cytokines and reduces virus replication and clinical manifestations of influenza virus infection in a mouse model.