Journal
JOURNAL OF NUTRITION
Volume 136, Issue 10, Pages 2611-2616Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jn/136.10.2611
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Funding
- NHLBI NIH HHS [HL42630] Funding Source: Medline
- NIAID NIH HHS [AI055050] Funding Source: Medline
- NIDDK NIH HHS [DK56350] Funding Source: Medline
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This study was designed to determine the effects of vitamin C deficiency on the immune response to infection with influenza virus. L-Gulono-gamma-lactone oxidase gene-inactivated mice (gulo-/- mice) require vitamin C supplementation for survival. Five-wk-old male and female gulo-/- mice were provided water or water containing 1.67 mmol/L vitamin C for 3 wk before inoculation with influenza A/Bangkok/l/79. There were no differences in lung influenza virus titers between vitamin C-adequate and-deficient mice; however, lung pathology in the vitamin C-deficient mice was greater at 1 and 3 d after infection but less at d 7 compared with vitamin C-adequate mice. Male vitamin C-deficient mice had higher expression of mRNA for regulated upon activation normal T expressed and secreted (RANTES), IL-1 beta, and TNF-alpha in the lungs at d 1 after infection compared with male controls. However, at d 3 after infection, male vitamin C-deficient mice had less expression of mRNA for RANTES, monocyte chemotactic protein-1 (MCP-1), and IL-12 compared with male controls. None of these differences were observed in female mice. Vitamin C-deficient male mice also had greater nuclear factor-kappa B activation as early as 1 d after infection compared with male controls. These data suggest that vitamin C is required for an adequate immune response in limiting lung pathology after influenza virus infection.
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