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].