SARS-CoV-2-triggered neutrophil extracellular traps mediate COVID-19 pathology

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Flavio Protasio Veras, Marjorie Cornejo Pontelli, Camila Meirelles Silva, Juliana E Toller-Kawahisa, Mikhael de Lima, Daniele Carvalho Nascimento, Ayda Henriques Schneider, Diego Caetité, Lucas Alves Tavares, Isadora M Paiva, Roberta Rosales, David Colón, Ronaldo Martins, Italo Araujo Castro, Glaucia M Almeida, Maria Isabel Fernandes Lopes, Maíra Nilson Benatti, Letícia Pastorelli Bonjorno, Marcela Cavichioli Giannini, Rodrigo Luppino-Assad, Sérgio Luna Almeida, Fernando Vilar, Rodrigo Santana, Valdes R Bollela, Maria Auxiliadora-Martins, Marcos Borges, Carlos Henrique Miranda, Antônio Pazin-Filho, Luis Lamberti P da Silva, Larissa Dias Cunha, Dario S Zamboni, Felipe Dal-Pizzol, Luiz O Leiria, Li Siyuan, Sabrina Batah, Alexandre Fabro, Thais Mauad, Marisa Dolhnikoff, Amaro Duarte-Neto, Paulo Saldiva, Thiago Mattar Cunha, José Carlos Alves-Filho, Eurico Arruda, Paulo Louzada-Junior, Renê Donizeti Oliveira, Fernando Queiroz Cunha

期刊 J Exp Med
影响因子 10.6
起止号 2020 Dec 7;217(12):e20201129.
种属 Rhesus,Cynomolgus,Dog
技术平台流式
应用领域呼吸系统
研究方向呼吸系统
细胞类型粒细胞
疾病类型新冠
检测蛋白 CD14
doi doi: 10.1084/jem.20201129.

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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Abstract