International journal of molecular sciences

2021-06-14

Iliadi V; Konstantinidou I; Aftzoglou K; Iliadis S; Konstantinidis TG; Tsigalou C

Medical School, Izhevsk State Medical Academy, Kommunarov Street 281, 426034 Izhevsk, Russia.; Medical School, University of Patras, Rio, 26504 Patra, Greece.; Medical School, Comenius University, Spitalska 24, 81372 Bratislava, Slovakia.; Medical School, Izhevsk State Medical Academy, Kommunarov Street 281, 426034 Izhevsk, Russia.; Blood Transfusion Center, University General Hospital of Alexandroupolis Dragana Campus, 68100 Alexandroupolis, Greece.; Laboratory of Microbiology, Democritus University of Thrace, Dragana Campus, 68100 Alexandroupolis, Greece.

Previous studies have shown that COVID-19 leads to thrombotic complications, which have been associated with high morbidity and mortality rates. Neutrophils are the largest population of white blood cells and play a pivotal role in innate immunity. During an infection, neutrophils migrate from circulation to the infection site, contributing to killing pathogens. This mechanism is regulated by chemokines such as IL-8. Moreover, it was shown that neutrophils play an important role in thromboinflammation. Through a diverse repertoire of mechanisms, neutrophils, apart from directly killing pathogens, are able to activate the formation of thrombi. In COVID-19 patients, neutrophil activation promotes neutrophil extracellular trap (NET) formation, platelet aggregation, and cell damage. Furthermore, neutrophils participate in the pathogenesis of endothelitis. Overall, this review summarizes recent progress in research on the pathogenesis of COVID-19, highlighting the role of the prothrombotic action of neutrophils in NET formation.