Israel Institute for Biological Research, Ness Ziona P.O. Box 19, Israel.
Department of Biological Regulation, Weizmann Institute of Science, Herzel 234, Rehovot P.O. Box 26, Israel.
Viruses. 2022 Jul 26;14(8):1627. doi: 10.3390/v14081627.
The COVID-19 pandemic caused by the SARS-CoV-2 infection induced lung inflammation characterized by cytokine storm and fulminant immune response of both resident and migrated immune cells, accelerating alveolar damage. In this work we identified members of the matrix metalloprotease (MMPs) family associated with lung extra-cellular matrix (ECM) destruction using K18-hACE2-transgenic mice (K18-hACE2) infected intranasally with SARS-CoV-2. Five days post infection, the lungs exhibited overall alveolar damage of epithelial cells and massive leukocytes infiltration. A substantial pulmonary increase in MMP8, MMP9, and MMP14 in the lungs post SARS-CoV-2 infection was associated with degradation of ECM components including collagen, laminin, and proteoglycans. The process of tissue damage and ECM degradation during SARS-CoV-2 lung infection is suggested to be associated with activity of members of the MMPs family, which in turn may be used as a therapeutic intervention.
由 SARS-CoV-2 感染引起的 COVID-19 大流行导致肺部炎症,其特征是细胞因子风暴和常驻及迁移免疫细胞的剧烈免疫反应,加速了肺泡损伤。在这项工作中,我们使用 K18-hACE2 转基因小鼠(K18-hACE2)鉴定了与肺细胞外基质(ECM)破坏相关的基质金属蛋白酶(MMPs)家族成员,这些小鼠经鼻腔感染了 SARS-CoV-2。感染后 5 天,肺部表现出上皮细胞的整体肺泡损伤和大量白细胞浸润。SARS-CoV-2 感染后肺部 MMP8、MMP9 和 MMP14 的大量增加与 ECM 成分的降解有关,包括胶原、层粘连蛋白和糖胺聚糖。SARS-CoV-2 肺部感染过程中的组织损伤和 ECM 降解与 MMPs 家族成员的活性有关,这反过来可能被用作治疗干预措施。