Targeting potential drivers of COVID-19: Neutrophil extracellular traps

The Journal focuses on Infectious disease and host defense. Coronavirus disease 2019 (COVID-19) is a novel, viral-induced respiratory disease that in ∼10–15% of patients progresses to acute respiratory distress syndrome (ARDS) triggered by a cytokine storm. In this Perspective, autopsy results and literature are presented supporting the hypothesis that a little known yet powerful function of neutrophils—the ability to form neutrophil extracellular traps (NETs)—may contribute to organ damage and mortality in COVID-19. We show lung infiltration of neutrophils in an autopsy specimen from a patient who succumbed to COVID-19. We discuss prior reports linking aberrant NET formation to pulmonary diseases, thrombosis, mucous secretions in the airways, and cytokine production. If our hypothesis is correct, targeting NETs directly and/or indirectly with existing drugs may reduce the clinical severity of COVID-19. Patients with severe coronavirus disease 2019 (COVID-19)–associated pneumonitis and/or acute respiratory distress syndrome (ARDS) have increased pulmonary inflammation, thick mucous secretions in the airways, elevated levels of serum pro-inflammatory cytokines, extensive lung damage, and micro thrombosis.
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