Targeting potential drivers of COVID-19: Neutrophil extracellular traps

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 lit...

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Published inThe Journal of experimental medicine Vol. 217; no. 6
Main Authors Barnes, Betsy J., Adrover, Jose M., Baxter-Stoltzfus, Amelia, Borczuk, Alain, Cools-Lartigue, Jonathan, Crawford, James M., Daßler-Plenker, Juliane, Guerci, Philippe, Huynh, Caroline, Knight, Jason S., Loda, Massimo, Looney, Mark R., McAllister, Florencia, Rayes, Roni, Renaud, Stephane, Rousseau, Simon, Salvatore, Steven, Schwartz, Robert E., Spicer, Jonathan D., Yost, Christian C., Weber, Andrew, Zuo, Yu, Egeblad, Mikala
Format Journal Article
LanguageEnglish
Published United States Rockefeller University Press 01.06.2020
Subjects
Betacoronavirus
Coronavirus Infections - complications
Coronavirus Infections - pathology
COVID-19
Cytokines - metabolism
Extracellular Traps
Humans
Infectious Disease and Host Defense
Lung Diseases - etiology
Lung Diseases - metabolism
Lung Diseases - pathology
Neutrophils - pathology
Pandemics
Pneumonia, Viral - complications
Pneumonia, Viral - pathology
SARS-CoV-2
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Summary: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.
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Disclosures: M.R. Looney reported "other" from Neutrolis outside the submitted work. R.E. Schwartz is a Sponsored Advisory Board Member for Miromatrix Inc. J.D. Spicer reported personal fees from Bristol Myers Squibb, personal fees from Astra Zeneca, personal fees from Merck, personal fees from Trans-Hit Bio, and non-financial support from Astra Zeneca outside the submitted work. C.C. Yost reports a grant from PEEL Therapeutics, Inc. during the conduct of the study; in addition, C.C. Yost authors a US patent (patent no. 10,232,023 B2) held by the University of Utah for the use of NET-inhibitory peptides for "treatment of and prophylaxis against inflammatory disorders." PEEL Therapeutics, Inc. has exclusive licensing rights. M. Egeblad reported "other" from Santhera during the conduct of the study; and consulted for CytomX in 2019. No other disclosures were reported.
ISSN:0022-1007
1540-9538
1540-9538
DOI:10.1084/jem.20200652