In addition, they also found that the overactivation of T cells and the decrease in the cell counts may explain the occurrence of cytokine storms and, to some degree, the severe immune-medicated injury. All these results indicated that decreasing cytokine storms and immunogenetic damage may be the main treatment option for critically ill patients with COVID-19. Vitamin C (VC), a common and necessary nutrient, is also an antioxidant. In addition to its role in the metabolism of the human body, including energy transformation, collagen biosynthesis and repair, adrenal steroid and catecholamine production, iron absorption and so on, 14–19 VC also possesses antimicrobial properties-thus reducing the risk of infections-and immunomodulatory functions, particularly in high concentrations.

It can inhibit the activation of nuclear factor kappa-B (NFκB), which is a primary proinflammatory transcription factor, and plays a pivotal role in overall immunity, including the genetic regulation of chemokines, cytokines, adhesion molecules, inflammatory mediators and apoptosis inhibitors.ġ4 First, VC plays a crucial role in immunomodulation. 20 VC can inhibit the production of IL-6 and tumor necrosis factor alpha (TNF-α), 21 22 and this effect appears to be a dose dependent. 21 VC can reduce GM-CSF signalling responses, 23 functioning as a regulator of cytokine redox-signal transduction in host defence cells and having a possible role in controlling inflammatory responses. In addition, high-dose VC can regulate the proliferation and function of T cells, B cells and natural killer (NK) cells. 24–27 This may help inhibit the progression of cytokine storms and improve the host’s immunity. Second, previous studies 22 demonstrated that VC can inhibit oxidative stress, an important part of the innate immune response to viral respiratory infection 28 29 and contributes to lung injury and barrier dysfunction. 28 Oxidative stress may also play a role in the mechanism of COVID-19. 29 It has been reported that VC can repair oxidative damage in human bronchial epithelium by modulating reactive oxygen species (ROS) generation and inflammatory expression 30 and can prevent ROS-induced lung damage.

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