Interleukin 6: A biomarker for COVID-19 progression

Abstract

COVID-19 was discovered in China for the first time in December 2019 and was declared a pandemic by the World Health Organization on March 11, 2020. Due to its rapid geographic expansion over the last three years, it has now become a global health issue. The infection is caused by SARS-CoV-2, which is obtained from a zoonotic source and transmitted directly or through contact. Following exposure, the immune system becomes hyperactive resulting in the production of pro-inflammatory cytokines, particularly interleukin-6 (IL-6), a naturally occurring pleiotropic cytokine that plays a significant role in respiratory failure and multi-organ dysfunction. This massive inflammatory phenomenon is reminiscent of cytokine release syndrome (CRS) or "cytokine storm", which may be at the root of many severe complications. In fact, serum IL-6 levels are significantly high in patients with severe Covid-19 disease. The goal of treatment is to change the cytokine's concentration or activity. Interleukin-6 production could be inhibited, reducing inflammation and so serving as a therapeutic target. anti-interleukin-6 receptor monoclonal antibodies have been proven to reduce the severity of COVID-19 in clinical trials aimed at clarifying the function of immunoregulation. As a result, the Il-6 assay is a reliable predictor of morbidity and mortality at the time of infection diagnosis. The aim of our study is to highlight the role of interleukin 6 as biomarker of the COVID- 19 progression.

Keywords: Biomarker; COVID-19; Cytokine storm; Interleukin-6; Monoclonal antibodies; SARS-CoV-2.

Fig. 1

In healthy state, the Angiotensin II –Angiotensin I Receptor axis and the Angiotensin 1–7-Mas receptor axis are in a state of dynamic equilibrium to maintain the blood pressure. The former causes an inflammatory response while the latter suppresses inflammatory responses. In SARS-CoV-2 infected state, viral binding to ACE2 renders it unavailable to bind to Angiotensin II causing an imbalance between the two axes and a shift towards the proinflammatory functions .