COVID-19 is an infectious and inflammatory disease caused by SARS-CoV-2 (Severe Acute Respiratory Syndrome-Coronavirus-2) that might progress to severe illness in humans, characterized by excessive pulmonary and systemic inflammation. Exacerbated production of inflammatory cytokines and cell death contributes to disease aggravation and the inflammasomes take a central stage in this process. Activation of the NLRP3 has been demonstrated in macrophages and monocytes infected in vitro, in mouse models of infection, and in cells and lungs of severe cases of COVID-19. It is still not clear how SARS-CoV-2 activates the NLRP3 inflammasome, and recent reports suggest that the virus engages the CASP4/11 (Caspase 4/11)-mediated noncanonical activation of NLRP3. In this review, we discuss the recent data regarding the activation of NLRP3 inflammasome by SARS-CoV-2 and their participation in the development of severe cases of COVID-19.

COVID-19 是一种由 SARS-CoV-2（严重急性呼吸综合征-冠状病毒-2）引起的传染性和炎症性疾病，可能会发展为人类严重疾病，其特征是过度的肺部和全身炎症。炎症细胞因子和细胞死亡的加剧会导致疾病恶化，而炎症小体在这一过程中发挥着核心作用。NLRP3 的激活已在体外感染的巨噬细胞和单核细胞、感染的小鼠模型以及 COVID-19 重症病例的细胞和肺部中得到证实。目前尚不清楚 SARS-CoV-2 如何激活NLRP3 炎症小体，最近的报告表明该病毒参与了 CASP4/11 (Caspase 4/11) 介导的 NLRP3 的非典型激活。在这篇综述中，我们讨论了有关 SARS-CoV-2 激活 NLRP3 炎性体及其参与 COVID-19 重症病例发展的最新数据。