SARS-CoV-2 engages inflammasome and pyroptosis in human primary monocytes.
André C FerreiraVinicius Cardoso SoaresIsaclaudia G de Azevedo-QuintanilhaSuelen da Silva Gomes DiasNatalia Fintelman-RodriguesCarolina Q SacramentoMayara MattosCaroline S de FreitasJairo R TemerozoLívia TeixeiraEugenio Damaceno HottzEster de A BarretoCamila R R PãoLohanna PalhinhaMilene MirandaDumith Chequer Bou-HabibFernando A BozzaPatrícia T BozzaThiago Moreno L SouzaPublished in: Cell death discovery (2021)
Infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with leukopenia and uncontrolled inflammatory response in critically ill patients. A better comprehension of SARS-CoV-2-induced monocyte death is essential for the identification of therapies capable to control the hyper-inflammation and reduce viral replication in patients with 2019 coronavirus disease (COVID-19). Here, we show that SARS-CoV-2 engages inflammasome and triggers pyroptosis in human monocytes, experimentally infected, and from patients under intensive care. Pyroptosis associated with caspase-1 activation, IL-1ß production, gasdermin D cleavage, and enhanced pro-inflammatory cytokine levels in human primary monocytes. At least in part, our results originally describe mechanisms by which monocytes, a central cellular component recruited from peripheral blood to respiratory tract, succumb to control severe COVID-19.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- peripheral blood
- coronavirus disease
- endothelial cells
- dendritic cells
- inflammatory response
- respiratory tract
- pluripotent stem cells
- nlrp inflammasome
- end stage renal disease
- chronic kidney disease
- prognostic factors
- newly diagnosed
- toll like receptor
- patient reported outcomes
- induced apoptosis