Inflammatory response to COVID-19

ABSTRACT

Innate immune and inflammatory responses play a major role in the pathogenesis of the COVID-19 disease. In normal conditions, they are necessary for the effective clearance of SARS-CoV-2. However, an uncontrolled pro-inflammatory response results in severe COVID-19 disease, acute respiratory distress syndrome, and cytokine storm. Quantitative analysis of the cytokines is useful for COVID-19 disease severity and mortality risk evaluation. According to literature data, SARS-CoV-2 infected patients have significantly higher concentrations of interleukin (IL)-6, IL-10, IL-8, interferon (IFN)-g, tumor necrosis factor (TNF)-a, and monocyte chemoattractant protein (MCP)-1 compared to healthy controls. Severe-critical COVID-19 is discriminated from mild-moderate disease by significantly higher concentrations of IL-6, IL-8, IFN-g-inducible protein (IP)-10, TNF-a, IL-10, and MCP-1, while COVID-19 patient mortality is associated with significantly higher concentrations of IL-6, IFN-g, IP-10, and IL-10. Patients treated in the specialized COVID-19 department of the Hospital of Lithuanian University of Health Sciences Kauno klinikos had significantly higher concentrations of IL-6, IL-10, IFN-g, and neutrophil-gelatinase-associated lipocalin than healthy individuals. Deceased patients had a significantly higher concentration of IL-6 compared to those who recovered. Regarding routinely performed inflammatory marker assays, severe, critical and deceased COVID-19 patients had significantly higher neutrophil-lymphocyte ratio and ferritin concentration compared to mild-moderate and recovered patients, respectively. Deceased patients additionally had a significantly higher white blood cell count and C reactive protein concentration compared to those who recovered. To conclude, hyper-inflammation is the main factor influencing COVID-19 disease severity and mortality. IL-6, IL-10, and routinely tested inflammatory markers could be used to predict unfavorable outcomes of COVID-19.