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.