Cytokine storm in COVID-19
Cytokine release plays a vital role in the immune-pathology against a virus, but over-expressions of immune mediators may cause severe damage to the human organ systems. Patients suffering from COVID-19 have been diagnosed with overexpression of monocyte chemo-attractant protein (MCP-1), IFN-γ, IP-10, and IL-1β. These pro-inflammatory cytokines may cause activation of responses from the T-helper type 1 cells (Th1). COVID-19 patients have also shown high levels of cytokines secreted by Th2 cells like IL-10 and IL-4.
These two cytokines are involved in inhibition of the inflammatory response. Furthermore, the levels of IL-6 and IL-2 R, obtained from serum, depict a positive correlation with the disease severity, which means they are highest in patients who are critically ill and lowest in ordinary patients. Another study on patients in Wuhan, China, compared the COVID-19 patients from the general wards and the intensive care units (ICUs). The latter were reported to exhibit increased levels of serum IP-10, macrophage inflammatory protein-1A, granulocyte colony-stimulating factor and TNF-α. The above studies act as evidence of the positive correlation between the ‘cytokine storm’ and COVID-19 progression [6].
The mechanism of cytokine storm syndrome depends on the imbalance of pro-inflammatory and anti-inflammatory process and the interaction of specific cells and cytokines, resulting in immune regulation disorder. Cytokines can be markedly increased in patients with cytokine storm syndrome, which differ according to the heterogeneity of the disease. A previous study found that H5N1 infected patients had higher levels of interferon-gamma-induced protein-10 (IP-10), monocyte chemo-attractant protein 1 (MCP-1) and IL-8 than patients with seasonal H1N1 influenza. Moreover, it was confirmed that cytokines play an important role in the pathogenesis of severe CoV infection. Spleen and lymph node atrophy are observed in patients with COVID-19, while lymphadenopathy and splenomegaly are more common in other cytokine storm syndrome related diseases [7].