| Summary: | Abstract Coronavirus disease 2019 (COVID-19) is an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can lead to acute respiratory distress syndrome (ARDS), multi-organ failure and death, posing significant threat to human health. Studies have found that pathological mechanisms, such as cytokine storms caused by uncontrolled innate immune system activation, release of damage-associated molecular patterns during tissue injury and a high incidence of thrombotic events, are associated with the function and dysfunction of neutrophils. Specifically, the increased formation of low-density neutrophils (LDNs) and neutrophil extracellular traps (NETs) has been shown to be closely linked with the severity and poor prognosis in patients with COVID-19. Our work focuses on understanding the increased number, abnormal activation, lung tissue infiltration, and elevated neutrophil-to-lymphocyte ratio in the pathogenesis of COVID-19. We also explore the involvement of NETs and LDNs in disease progression and thrombosis formation, along with potential therapeutic strategies targeting neutrophil and NETs formation.
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