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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Exp+Med 2020 ; 217 (12): ä Nephropedia Template TP
Veras FP; Pontelli MC; Silva CM; Toller-Kawahisa JE; de Lima M; Nascimento DC; Schneider AH; Caetite D; Tavares LA; Paiva IM; Rosales R; Colon D; Martins R; Castro IA; Almeida GM; Lopes MIF; Benatti MN; Bonjorno LP; Giannini MC; Luppino-Assad R; Almeida SL; Vilar F; Santana R; Bollela VR; Auxiliadora-Martins M; Borges M; Miranda CH; Pazin-Filho A; da Silva LLP; Cunha LD; Zamboni DS; Dal-Pizzol F; Leiria LO; Siyuan L; Batah S; Fabro A; Mauad T; Dolhnikoff M; Duarte-Neto A; Saldiva P; Cunha TM; Alves-Filho JC; Arruda E; Louzada-Junior P; Oliveira RD; Cunha FQ
J Exp Med 2020[Dec]; 217 (12): ä PMID32926098show ga
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.