IL-32 is a Novel Regulator for Increasing Caspase-1 Gene Expression as a Proinflammatory in Early SARS-CoV-2 Infection

Objective: The aim of this study is to determine whether the levels of caspase-1 and IL-32 gene expression are associated with the severity and progression of COVID-19 and its correlation with other clinical and biological markers of infection. Materials and Methods: About 100 patients with coronavirus infectious disease (COVID-19) and 58 healthy individuals were enrolled to assess the gene expression of interleukin-32 (IL-32) and caspase-1 by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), with some emphasis on clinical and biological markers of disease like c-reactive protein, chemokine (CCL-2), and tumor protein (P53). Results: The finding showed that CCL-2 and P53 levels in patients showed a significant decrease (185 ng/L and 24.5 ng/mL) than in the control group (229 ng/L and 30 ng/mL) ( P = 0.001). The ratio of relative IL-32 and caspase-1 gene expression in COVID-19 patients compared to healthy control was 1.5 and 1.2, respectively. Although the 2 −∆∆Ct of IL-32 and caspase-1 expression showed no significant variation between the age group (≤45 and > 45 years), sex, and severity in patients and controls, nonstatistical increasing 2 −∆∆Ct means of IL-32 and caspase-1 in mild to moderate (17.1 and 13) than in severe (15 and 12.7) and critical (13.3 and 11.6) patients, respectively. The findings showed the CCL-2 levels were significantly correlated with the increase of IL-32 levels ( P < 0.05) and a significant decrease in the P53 level with caspase-1 increased expression ( P < 0.01). Conclusion: It is concluded that gene expression of IL-32 was a novel regulated caspase-1 increase expression in COVID-19 patients, especially CRP-positive patients. Moreover, the gene expression of IL-32 and caspase-1 as a biomarker may have a role in CCL-2 and P53 regulation to reduce COVID-19 risk.