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

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....

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Published inNutrients 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
LanguageEnglish
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
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Abstract 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.
AbstractList 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.
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) 2 D], 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 D 3 [25(OH)D 3 ], 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)D 3 and were challenged with the influenza virus. In the lungs of 25(OH)D 3 -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)D 3 -fed mice, while anti-inflammatory cytokines were not significantly upregulated. These results indicate that 25(OH)D 3 suppresses the production of inflammatory cytokines and reduces virus replication and clinical manifestations of influenza virus infection in a mouse model.
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.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.
Author Tsugawa, Naoko
Hayashi, Hirotaka
Ogasawara, Honami
Isoda, Norikazu
Sakoda, Yoshihiro
Okamatsu, Masatoshi
Matsuno, Keita
AuthorAffiliation 1 Laboratory of Microbiology, Faculty of Veterinary Medicine, Hokkaido University, Kita 18 Nishi 9, Kita-ku, Sapporo 060-0818, Japan; hayashihirotaka@vetmed.hokudai.ac.jp (H.H.); okamatsu@vetmed.hokudai.ac.jp (M.O.); matsuno@vetmed.hokudai.ac.jp (K.M.)
2 Department of Health and Nutrition, Faculty of Health and Nutrition, Osaka Shoin Woman’s University, Hishiyanishi 4-2-26, Higashiosaka 577-8550, Japan; ogasawara.honami@osaka-shoin.ac.jp (H.O.); tsugawa.naoko@osaka-shoin.ac.jp (N.T.)
4 Global Station of Zoonosis Control, Global Institution for Collaborative Research and Education (GI-CoRE), Hokkaido University, Sapporo 001-0020, Japan
3 Unit of Risk Analysis and Management, Research Center for Zoonosis Control, Hokkaido University, Kita 20 Nishi 10, Kita-ku, Sapporo 001-0020, Japan; isoda@czc.hokudai.ac.jp
AuthorAffiliation_xml – name: 1 Laboratory of Microbiology, Faculty of Veterinary Medicine, Hokkaido University, Kita 18 Nishi 9, Kita-ku, Sapporo 060-0818, Japan; hayashihirotaka@vetmed.hokudai.ac.jp (H.H.); okamatsu@vetmed.hokudai.ac.jp (M.O.); matsuno@vetmed.hokudai.ac.jp (K.M.)
– name: 3 Unit of Risk Analysis and Management, Research Center for Zoonosis Control, Hokkaido University, Kita 20 Nishi 10, Kita-ku, Sapporo 001-0020, Japan; isoda@czc.hokudai.ac.jp
– name: 4 Global Station of Zoonosis Control, Global Institution for Collaborative Research and Education (GI-CoRE), Hokkaido University, Sapporo 001-0020, Japan
– name: 2 Department of Health and Nutrition, Faculty of Health and Nutrition, Osaka Shoin Woman’s University, Hishiyanishi 4-2-26, Higashiosaka 577-8550, Japan; ogasawara.honami@osaka-shoin.ac.jp (H.O.); tsugawa.naoko@osaka-shoin.ac.jp (N.T.)
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  surname: Sakoda
  fullname: Sakoda, Yoshihiro
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Snippet 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...
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StartPage 2000
SubjectTerms Chromatography
Cytokines
Diet
Infections
Influenza
Kidneys
Lungs
Lymphocytes
Small intestine
Tumor necrosis factor-TNF
Vitamin D
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Title Oral Supplementation of the Vitamin D Metabolite 25(OH)D3 Against Influenza Virus Infection in Mice
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https://pubmed.ncbi.nlm.nih.gov/PMC7400405
Volume 12
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