Tissue damage from neutrophil-induced oxidative stress in COVID-19

Abstract

The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. We suggest that free radical scavengers could be beneficial for the most vulnerable patients.

Fig. 1. SARS-CoV-2 infection can lead to neutrophilia-induced ROS release.

a | In not at-risk individuals, an excess of reactive oxygen species (ROS) is counterbalanced by an increase in antioxidant defences. b | In subjects with impaired redox balance, ROS production is not properly controlled, leading to red blood cell (RBC) membrane peroxidation, which in turn perpetuates neutrophil activation. Excessive oxidative stress might be responsible for the alveolar damage, thrombosis and RBC dysregulation seen in COVID-19. Anti-oxidants and elastase inhibitors may have therapeutic potential.