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 in	The 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
Language	English
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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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.
AbstractList	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.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. 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. In this Perspective, autopsy results and literature are presented supporting the hypothesis that neutrophil extracellular traps (NETs) may contribute to organ damage and mortality in COVID-19. If correct, existing drugs that target NETs, although unspecific, may benefit COVID-19 patients. 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.
Author	Cools-Lartigue, Jonathan Weber, Andrew Baxter-Stoltzfus, Amelia Huynh, Caroline Crawford, James M. Knight, Jason S. Loda, Massimo Spicer, Jonathan D. Zuo, Yu Looney, Mark R. Salvatore, Steven Yost, Christian C. Rayes, Roni Schwartz, Robert E. Adrover, Jose M. Daßler-Plenker, Juliane Guerci, Philippe Borczuk, Alain McAllister, Florencia Barnes, Betsy J. Egeblad, Mikala Renaud, Stephane Rousseau, Simon
AuthorAffiliation	6 Centre Hospitalier Universitaire de Nancy, Nancy, France 14 Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Northwell Health, Manhasset, NY 12 Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, New York, NY 8 Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 10 Department of Clinical Cancer Prevention, University of Texas MD Anderson Cancer Center, Houston, TX 2 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 1 Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, The Feinstein Institutes for Medical Research & Departments of Molecular Medicine and Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY 11 Department of Medicine, McGill University & The Research Institute of the McGill University Health Centre, Montreal, Canada 4 Division of Thoracic and Upper GI Surgery, Department of Surgery, Montreal, Canada 7 Goo
AuthorAffiliation_xml	– name: 5 Department of Pathology and Laboratory Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, East Garden City, NY – name: 11 Department of Medicine, McGill University & The Research Institute of the McGill University Health Centre, Montreal, Canada – name: 4 Division of Thoracic and Upper GI Surgery, Department of Surgery, Montreal, Canada – name: 10 Department of Clinical Cancer Prevention, University of Texas MD Anderson Cancer Center, Houston, TX – name: 13 Department of Pediatrics, Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, UT – name: 1 Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, The Feinstein Institutes for Medical Research & Departments of Molecular Medicine and Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY – name: 7 Goodman Cancer Research Centre, McGill University, Montreal, Canada – name: 9 Department of Medicine, University of California, San Francisco, San Francisco, CA – name: 6 Centre Hospitalier Universitaire de Nancy, Nancy, France – name: 8 Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI – name: 3 Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY – name: 2 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY – name: 12 Division of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, New York, NY – name: 14 Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Northwell Health, Manhasset, NY
Author_xml	– sequence: 1 givenname: Betsy J. surname: Barnes fullname: Barnes, Betsy J. – sequence: 2 givenname: Jose M. surname: Adrover fullname: Adrover, Jose M. – sequence: 3 givenname: Amelia surname: Baxter-Stoltzfus fullname: Baxter-Stoltzfus, Amelia – sequence: 4 givenname: Alain orcidid: 0000-0001-6807-8064 surname: Borczuk fullname: Borczuk, Alain – sequence: 5 givenname: Jonathan surname: Cools-Lartigue fullname: Cools-Lartigue, Jonathan – sequence: 6 givenname: James M. orcidid: 0000-0002-8581-1093 surname: Crawford fullname: Crawford, James M. – sequence: 7 givenname: Juliane surname: Daßler-Plenker fullname: Daßler-Plenker, Juliane – sequence: 8 givenname: Philippe surname: Guerci fullname: Guerci, Philippe – sequence: 9 givenname: Caroline orcidid: 0000-0003-2101-8966 surname: Huynh fullname: Huynh, Caroline – sequence: 10 givenname: Jason S. orcidid: 0000-0003-0995-9771 surname: Knight fullname: Knight, Jason S. – sequence: 11 givenname: Massimo surname: Loda fullname: Loda, Massimo – sequence: 12 givenname: Mark R. orcidid: 0000-0003-0241-9190 surname: Looney fullname: Looney, Mark R. – sequence: 13 givenname: Florencia surname: McAllister fullname: McAllister, Florencia – sequence: 14 givenname: Roni orcidid: 0000-0001-7508-020X surname: Rayes fullname: Rayes, Roni – sequence: 15 givenname: Stephane surname: Renaud fullname: Renaud, Stephane – sequence: 16 givenname: Simon orcidid: 0000-0002-8773-575X surname: Rousseau fullname: Rousseau, Simon – sequence: 17 givenname: Steven orcidid: 0000-0001-7237-2696 surname: Salvatore fullname: Salvatore, Steven – sequence: 18 givenname: Robert E. orcidid: 0000-0002-5417-5995 surname: Schwartz fullname: Schwartz, Robert E. – sequence: 19 givenname: Jonathan D. orcidid: 0000-0003-2708-1309 surname: Spicer fullname: Spicer, Jonathan D. – sequence: 20 givenname: Christian C. surname: Yost fullname: Yost, Christian C. – sequence: 21 givenname: Andrew orcidid: 0000-0001-9800-3709 surname: Weber fullname: Weber, Andrew – sequence: 22 givenname: Yu surname: Zuo fullname: Zuo, Yu – sequence: 23 givenname: Mikala orcidid: 0000-0002-3371-1445 surname: Egeblad fullname: Egeblad, Mikala
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/32302401$$D View this record in MEDLINE/PubMed
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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.
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Snippet	Coronavirus disease 2019 (COVID-19) is a novel, viral-induced respiratory disease that in ∼10–15% of patients progresses to acute respiratory distress syndrome... Coronavirus disease 2019 (COVID-19) is a novel, viral-induced respiratory disease that in ∼10-15% of patients progresses to acute respiratory distress syndrome... In this Perspective, autopsy results and literature are presented supporting the hypothesis that neutrophil extracellular traps (NETs) may contribute to organ...
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SubjectTerms	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
Title	Targeting potential drivers of COVID-19: Neutrophil extracellular traps
URI	https://www.ncbi.nlm.nih.gov/pubmed/32302401 https://www.proquest.com/docview/2391981633 https://pubmed.ncbi.nlm.nih.gov/PMC7161085
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