Fig. 2.

The clinical features of COVID-19 patients are resulting from simultaneous events, promoting complex crosstalk between immune components. When SARS-CoV-2 infect host cell through Spike protein binding with ACE2 receptor, a wave of PAMPs and DAMPs ensues, activating pathways that enable inflammasome activation and leads to cleavage of IL-1β and IL-18, creating pro-inflammatory signals and leads to airway inflammation. Consequently, occurs platelet activation, fibrin deposition, and NETs release, which promotes tissue damage. A cascade involving inflammasome assembly and inflammation leads to ARDS development