Coronavirus disease 2019 (COVID-19) is an infectious respiratory disorder caused by a new coronavirus called SARS-CoV-2. The pathophysiology of severe COVID-19 is associated with a “cytokine storm”, characterized by anomalous release of various pro-inflammatory cytokines which contribute to alveolar exudation and lung damage. Overproduction of the proinflammatory cytokines IL-1, IL-6, IL-8 and TNF-α and low of expression IFN-γ have been found in severe COVID-19 patients. The mechanism by which IL-32 exerts its signalling properties is unclear. IL-32 is a key modulator in the pathogenesis of various clinical conditions and is mostly induced by IL-8. IL-32 modulates important inflammatory pathways (including TNF-α, IL-6 and IL-1b), contributing to the pathogenesis of inflammatory diseases. A total of 64 COVID-19 patients, stratifying as mild moderate and severe patients and 27 healthy controls were consecutively enrolled in the study. Serum concentrations of biomarkers including IL-1β, IL-10, IFN-γ, TNF-α and IL-6 were quantified by bead-based multiplex analysis and Serum concentration of IL-8 and IL-32 were determined by enzyme-linked immunosorbent assay (ELISA) kits. Interestingly, among the blood parameters, neutrophil and lymphocyte counts were significantly lower in severe COVID-19 patients than in the other, on the contrary, CRP was significantly higher in severe patients than in other groups. The cytokines that best distinguished controls from COVID-19 patients were IL-8 and IL-32.The best model performance for severe group was obtained by the combination of IL-32, IL-6 and IFN-γ, and serum concentrations of CRP increased model performance, showing AUC=0.83. New insights into the cytokine storm in COVID-19 patients, highlighting specific cytokine signatures among patients with different severity of infection.
