Targeting potential drivers of COVID-19: Neutrophil extracellular traps
Betsy Barnes, José M. Adrover, Amelia Baxter-Stoltzfus, Alain Borczuk, Jonathan Cools‐Lartigue, James M. Crawford, Juliane Daßler‐Plenker, Philippe Guerci, Caroline Huynh, Jason S. Knight, Massimo Loda, Mark R. Looney, Florencia McAllister, Roni Rayes, Stéphane Renaud, Simon Rousseau, Steven Salvatore, Robert E. Schwartz, Jonathan Spicer, Christian C. Yost, Andrew Weber, Yu Zuo, Mikala Egeblad
Abstract
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.