4. CYTOKINE STORM
The cytokine storm during SARS-CoV-2 infection has been associated with the severity and mortality in COVID-19 patients. The impaired acquired immune responses and uncontrolled inflammatory innate responses to SARS-CoV-2 may cause cytokine storm (Hu, Huang & Yin, 2021; Thepmankorn et al., 2021). During SARS-CoV-2 infection, the interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) are the most frequently reported cytokines that are significantly increased (Qin et al., 2020; Thepmankorn et al., 2021). Other cytokines that are increased but not exclusively include granulocyte stimulating factor (G-CSF), interferon gamma-induced protein 10 (IP-10), monocyte chemoattractant protein (MCP)-1, MCP-3, macrophage inflammatory protein 1α (MIP-1A), cutaneous T-cell attracting chemokine (CTACK), IFN-γ, and TNF-α, and IL-1~10 and 18 (Hadjadj et al., 2020). To prevent cytokine storm should be an important strategic measure for the treatment of COVID-19 (Lariccia, Magi, Serfilippi, Toujani, Gratteri & Amoroso, 2020).
Corticosteroids have been used in COVID-19 pneumonia to reduce systemic inflammation; however, they may increase the risk of delayed viral elimination and secondary infection. Since cytokines are the effectors in the cytokine storm, the specific cytokine antagonists should reduce cytokine induced damage when they are used for the treatment of COVID-19. Either monoclonal antibodies against cytokines or pharmacological inhibitors of cytokines will fall into this category.