COVID-19 is a contagious disease that attacks many organs but the lungs are the main organs affected. The inflammasome activation results in the exacerbation of inflammatory response in infectious disease. The aim of this study is to investigate the formation and activity of the NLRP3 inflammasome complex and the histopathological changes caused by the coronavirus in the lung of deceased persons with COVID-19. In total, 10 corpses; 5 corpses with no history of any infectious diseases and COVID-19 and 5 corpses with the cause of death of COVID-19 were included in this study. Lung tissue samples were harvested during autopsy under safe conditions. Fresh tissues in each group were used to measure the genes expression and proteins level of NLRP3, ASC, Caspase-1, IL-1β, IL-6 and TNF-α and a routine hematoxylin and eosin staining was performed for histological assessment. Data are represented as the means ± SD. Statistical significance difference was accepted at a p-value less than 5%. The NLRP3, ASC, Caspase-1, IL-1β, IL-6 and TNF-α genes expression and proteins level were elevated in the lung of the COVID-19 group in comparison with the control group. Histological findings presented the increasing number of polymorphonuclear leukocytes, macrophages and also pulmonary fibrosis in the lungs of corpses with the cause of death of COVID-19. High expression of NLRP3 inflammasome components and its relation with the pathophysiology of the coronavirus-infected lung suggested that targeting the NLRP3 inflammasome could be helpful in achieving a more effective treatment in patients with COVID-19.

COVID-19 是一种传染性疾病，会攻击许多器官，但肺部是受影响的主要器官。炎性体激活导致传染病中炎症反应的加剧。本研究的目的是研究 NLRP3 炎性体复合物的形成和活性，以及​​冠状病毒引起的 COVID-19 死者肺组织病理学变化。总共有10具尸体；本研究纳入了 5 具没有任何传染病和 COVID-19 病史的尸体和 5 具死因为 COVID-19 的尸体。在安全条件下尸检期间采集肺组织样本。取各组新鲜组织检测NLRP3、ASC、Caspase-1、IL-1β、进行 IL-6 和 TNF-α 以及常规苏木精和伊红染色以进行组织学评估。数据表示为平均值±SD。在小于 5% 的 p 值下接受统计显着性差异。与对照组相比，COVID-19 组肺中 NLRP3、ASC、Caspase-1、IL-1β、IL-6 和 TNF-α 基因表达和蛋白水平升高。组织学结果表明，死因为 COVID-19 的尸体肺部多形核白细胞、巨噬细胞和肺纤维化数量不断增加。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。数据表示为平均值±SD。在小于 5% 的 p 值下接受统计显着性差异。与对照组相比，COVID-19 组肺中 NLRP3、ASC、Caspase-1、IL-1β、IL-6 和 TNF-α 基因表达和蛋白水平升高。组织学结果表明，死因为 COVID-19 的尸体肺部多形核白细胞、巨噬细胞和肺纤维化数量不断增加。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。数据表示为平均值±SD。在小于 5% 的 p 值下接受统计显着性差异。与对照组相比，COVID-19 组肺中 NLRP3、ASC、Caspase-1、IL-1β、IL-6 和 TNF-α 基因表达和蛋白水平升高。组织学结果表明，死因为 COVID-19 的尸体肺部多形核白细胞、巨噬细胞和肺纤维化数量不断增加。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。与对照组相比，COVID-19 组肺中 Caspase-1、IL-1β、IL-6 和 TNF-α 基因表达和蛋白水平升高。组织学结果表明，死因为 COVID-19 的尸体肺部多形核白细胞、巨噬细胞和肺纤维化数量不断增加。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。与对照组相比，COVID-19 组肺中 Caspase-1、IL-1β、IL-6 和 TNF-α 基因表达和蛋白水平升高。组织学结果表明，死因为 COVID-19 的尸体肺部多形核白细胞、巨噬细胞和肺纤维化数量不断增加。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。死因为 COVID-19 的尸体肺部的巨噬细胞和肺纤维化。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。死因为 COVID-19 的尸体肺部的巨噬细胞和肺纤维化。NLRP3 炎症小体成分的高表达及其与冠状病毒感染肺部病理生理学的关系表明，靶向 NLRP3 炎症小体可能有助于对 COVID-19 患者实现更有效的治疗。