Yejin Kim 1Hyemin KimSeyeon BaeJiwon ChoiSun Young LimNaeun LeeJoo Myung KongYoung-Il HwangJae Seung KangWang Jae Lee

Immune Netw. 2013 Apr;13(2):70-4.

doi: 10.4110/in.2013.13.2.70. Epub 2013 Apr 30.

Abstract

L-ascorbic acid (vitamin C) is one of the well-known anti-viral agents, especially to influenza virus. Since the in vivo anti-viral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-α/β, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-α/β, were increased in the lung. Taken together, vitamin C shows in vivo anti-viral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-α/β.

 

Crit Care. 2020; 24: 133.

Crit Care. 2020; 24: 133.

Published online 2020 Apr 7. doi: 10.1186/s13054-020-02851-4

 

Published online 2020 Apr 7. doi: 10.1186/s13054-020-02851-4