SARS-CoV-2–triggered neutrophil extracellular traps mediate COVID-19 pathology
Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigate...
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| Published in | The Journal of experimental medicine Vol. 217; no. 12 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Rockefeller University Press
07.12.2020
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled. The concentration of NETs was augmented in plasma, tracheal aspirate, and lung autopsies tissues from COVID-19 patients, and their neutrophils released higher levels of NETs. Notably, we found that viable SARS-CoV-2 can directly induce the release of NETs by healthy neutrophils. Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus replication, and PAD-4. Finally, NETs released by SARS-CoV-2–activated neutrophils promote lung epithelial cell death in vitro. These results unravel a possible detrimental role of NETs in the pathophysiology of COVID-19. Therefore, the inhibition of NETs represents a potential therapeutic target for COVID-19. |
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| AbstractList | Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled. The concentration of NETs was augmented in plasma, tracheal aspirate, and lung autopsies tissues from COVID-19 patients, and their neutrophils released higher levels of NETs. Notably, we found that viable SARS-CoV-2 can directly induce the release of NETs by healthy neutrophils. Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus replication, and PAD-4. Finally, NETs released by SARS-CoV-2–activated neutrophils promote lung epithelial cell death in vitro. These results unravel a possible detrimental role of NETs in the pathophysiology of COVID-19. Therefore, the inhibition of NETs represents a potential therapeutic target for COVID-19. The knowledge of COVID-19 pathophysiology is pivotal for the discovery of effective treatments. Here, we described that SARS-CoV-2 triggers the release of ACE2-depended neutrophil extracellular traps (NETs) that mediate lung pathology, supporting the use of NETs inhibitors for COVID-19 treatment. Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled. The concentration of NETs was augmented in plasma, tracheal aspirate, and lung autopsies tissues from COVID-19 patients, and their neutrophils released higher levels of NETs. Notably, we found that viable SARS-CoV-2 can directly induce the release of NETs by healthy neutrophils. Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus replication, and PAD-4. Finally, NETs released by SARS-CoV-2–activated neutrophils promote lung epithelial cell death in vitro. These results unravel a possible detrimental role of NETs in the pathophysiology of COVID-19. Therefore, the inhibition of NETs represents a potential therapeutic target for COVID-19. Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled. The concentration of NETs was augmented in plasma, tracheal aspirate, and lung autopsies tissues from COVID-19 patients, and their neutrophils released higher levels of NETs. Notably, we found that viable SARS-CoV-2 can directly induce the release of NETs by healthy neutrophils. Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus replication, and PAD-4. Finally, NETs released by SARS-CoV-2-activated neutrophils promote lung epithelial cell death in vitro. These results unravel a possible detrimental role of NETs in the pathophysiology of COVID-19. Therefore, the inhibition of NETs represents a potential therapeutic target for COVID-19.Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled. The concentration of NETs was augmented in plasma, tracheal aspirate, and lung autopsies tissues from COVID-19 patients, and their neutrophils released higher levels of NETs. Notably, we found that viable SARS-CoV-2 can directly induce the release of NETs by healthy neutrophils. Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus replication, and PAD-4. Finally, NETs released by SARS-CoV-2-activated neutrophils promote lung epithelial cell death in vitro. These results unravel a possible detrimental role of NETs in the pathophysiology of COVID-19. Therefore, the inhibition of NETs represents a potential therapeutic target for COVID-19. |
| Author | Bollela, Valdes R. Schneider, Ayda Henriques Silva, Camila Meirelles Vilar, Fernando Cunha, Thiago Mattar Dolhnikoff, Marisa Luppino-Assad, Rodrigo Dal-Pizzol, Felipe Borges, Marcos Pazin-Filho, Antônio de Lima, Mikhael Benatti, Maíra Nilson Veras, Flavio Protasio Almeida, Glaucia M. Bonjorno, Letícia Pastorelli Mauad, Thais Duarte-Neto, Amaro Zamboni, Dario S. Lopes, Maria Isabel Fernandes Siyuan, Li Paiva, Isadora M. Miranda, Carlos Henrique Almeida, Sérgio Luna Cunha, Larissa Dias Castro, Italo Araujo Giannini, Marcela Cavichioli Auxiliadora-Martins, Maria Martins, Ronaldo Louzada-Junior, Paulo Rosales, Roberta Nascimento, Daniele Carvalho Leiria, Luiz O. Batah, Sabrina Arruda, Eurico Saldiva, Paulo Alves-Filho, José Carlos Colón, David Oliveira, Renê Donizeti Santana, Rodrigo Tavares, Lucas Alves da Silva, Luis Lamberti P. Fabro, Alexandre Pontelli, Marjorie Cornejo Caetité, Diego Cunha, Fernando Queiroz Toller-Kawahisa, Juliana E. |
| AuthorAffiliation | 8 Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, Santa Catarina, Brazil 2 Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 3 Virology Research Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 1 Center of Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 6 Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 4 Department of Cell and Molecular Biology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 5 Divisions of Clinical Immunology, Emergency, Infectious Diseases and Intensive Care Unit, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil 7 Department Path |
| AuthorAffiliation_xml | – name: 2 Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 3 Virology Research Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 5 Divisions of Clinical Immunology, Emergency, Infectious Diseases and Intensive Care Unit, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 7 Department Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil – name: 1 Center of Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 4 Department of Cell and Molecular Biology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 6 Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil – name: 8 Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, Santa Catarina, Brazil |
| Author_xml | – sequence: 1 givenname: Flavio Protasio orcidid: 0000-0002-6222-4064 surname: Veras fullname: Veras, Flavio Protasio – sequence: 2 givenname: Marjorie Cornejo orcidid: 0000-0003-3173-5977 surname: Pontelli fullname: Pontelli, Marjorie Cornejo – sequence: 3 givenname: Camila Meirelles orcidid: 0000-0001-8185-4435 surname: Silva fullname: Silva, Camila Meirelles – sequence: 4 givenname: Juliana E. orcidid: 0000-0001-7323-5036 surname: Toller-Kawahisa fullname: Toller-Kawahisa, Juliana E. – sequence: 5 givenname: Mikhael orcidid: 0000-0002-9377-0340 surname: de Lima fullname: de Lima, Mikhael – sequence: 6 givenname: Daniele Carvalho orcidid: 0000-0002-0620-339X surname: Nascimento fullname: Nascimento, Daniele Carvalho – sequence: 7 givenname: Ayda Henriques orcidid: 0000-0003-2474-2773 surname: Schneider fullname: Schneider, Ayda Henriques – sequence: 8 givenname: Diego orcidid: 0000-0003-3916-6748 surname: Caetité fullname: Caetité, Diego – sequence: 9 givenname: Lucas 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surname: Louzada-Junior fullname: Louzada-Junior, Paulo – sequence: 45 givenname: Renê Donizeti orcidid: 0000-0003-0229-6864 surname: Oliveira fullname: Oliveira, Renê Donizeti – sequence: 46 givenname: Fernando Queiroz orcidid: 0000-0003-4755-1670 surname: Cunha fullname: Cunha, Fernando Queiroz |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32926098$$D View this record in MEDLINE/PubMed |
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| Title | SARS-CoV-2–triggered neutrophil extracellular traps mediate COVID-19 pathology |
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