[Progress in the relationship between NLRP3 inflammasome and lung injury in COVID-19]

Severe inflammatory responses are considered responsible for acute lung damage in COVID-19. SARS-CoV-2 enters lung cells via ACE2, and the NLR family pyrin domain containing 3 (NLRP3) inflammasome and the pro-caspase-1 are then activated, followed by release of mature IL-1β and IL-18 and other inflammatory cytokines, thereby leading to inflammation and apoptosis. This inflammatory process induces syndromes such as inflammatory cell infiltration, congestion, and edema in the lungs of COVID-19 patients. Some severe cases reported complications including acute respiratory distress syndrome (ARDS) and diffuse intravascular coagulation (DIC). There is no specific drug available for the treatment of COVID-19 at present. MCC950, colchicine and other NLRP3 inflammasome inhibitors, have been widely used in the treatment of various inflammatory diseases, and are currently in clinical trials for the treatment of COVID-19 patients. Here we reviewed the pathogenesis of COVID-19 and the SARS-CoV activation pathway of NLRP3 inflammasome, in order to reveal the role and mechanism of NLRP3 inflammasome in the process of SARS-CoV-2 infection, and provide a theoretical basis for the development of related targeted drugs.