Main Body

Studies have shown that SARS‐CoV‐2 causes the release of pro‐inflammatory cytokines such as interleukin (IL)‐6, IL‐1β and tumor necrosis factor (TNF)‐α which are mediators of lung inflammation, lung damage, fever, and fibrosis. Additionally, various chemokines have been found to play an important role in the disease progression. A plethora of pro‐inflammatory cytokines “cytokine storm” has been observed in severe cases of SARS‐CoV‐2 infection leading to acute respiratory distress syndrome (ARDS) and pneumonia that may prove fatal. To counteract cytokine storm‐inducing lung inflammation, several promising immunomodulatory approaches are being investigated in numerous clinical trials. However, the benefits of using these strategies should outweigh the risks involved as the use of certain immunosuppressive approaches might lead the host susceptible to secondary bacterial infections.