Campos-Gomez Javier, Petty Courtney Fernandez, Mazur Marina, Tang Liping, Solomon George M, Joseph Reny, Li Qian, Lever Jacelyn E Peabody, Hussain Shah, Harrod Kevin, Onuoha Ezinwanne, Kim Harrison, Rowe Steven M
Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama.
bioRxiv. 2023 Feb 1:2023.01.30.526308. doi: 10.1101/2023.01.30.526308.
The coronavirus disease (COVID-19) pandemic, caused by SARS-CoV-2 coronavirus, is devastatingly impacting human health. A prominent component of COVID-19 is the infection and destruction of the ciliated respiratory cells, which perpetuates dissemination and disrupts protective mucociliary transport (MCT) function, an innate defense of the respiratory tract. Thus, drugs that augment MCT could improve barrier function of the airway epithelium, reduce viral replication and, ultimately, COVID-19 outcomes. We tested five agents known to increase MCT through distinct mechanisms for activity against SARS-CoV-2 infection using a model of human respiratory epithelial cells terminally differentiated in an air/liquid interphase. Three of the five mucoactive compounds tested showed significant inhibitory activity against SARS-CoV-2 replication. An archetype mucoactive agent, ARINA-1, blocked viral replication and therefore epithelial cell injury, thus, it was further studied using biochemical, genetic and biophysical methods to ascertain mechanism of action via improvement of MCT. ARINA-1 antiviral activity was dependent on enhancing the MCT cellular response, since terminal differentiation, intact ciliary expression and motion was required for ARINA-1-mediated anti-SARS-CoV2 protection. Ultimately, we showed that improvement of cilia movement was caused by ARINA-1-mediated regulation of the redox state of the intracellular environment, which benefited MCT. Our study indicates that Intact MCT reduces SARS-CoV-2 infection, and its pharmacologic activation may be effective as an anti-COVID-19 treatment.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的冠状病毒病(COVID-19)大流行正在对人类健康造成毁灭性影响。COVID-19的一个突出特征是纤毛呼吸细胞的感染和破坏,这使得病毒传播持续存在,并破坏了保护性黏液纤毛运输(MCT)功能,而MCT功能是呼吸道的一种固有防御机制。因此,增强MCT的药物可以改善气道上皮的屏障功能,减少病毒复制,并最终改善COVID-19的病情。我们使用在气液界面终末分化的人呼吸道上皮细胞模型,测试了五种已知通过不同机制增加MCT的药物对SARS-CoV-2感染的活性。所测试的五种黏液活性化合物中有三种对SARS-CoV-2复制表现出显著的抑制活性。一种典型的黏液活性药物ARINA-1阻断了病毒复制,从而防止了上皮细胞损伤,因此,我们进一步使用生化、遗传和生物物理方法对其进行研究,以确定其通过改善MCT发挥作用的机制。ARINA-1的抗病毒活性依赖于增强MCT细胞反应,因为ARINA-1介导的抗SARS-CoV-2保护作用需要终末分化、完整的纤毛表达和运动。最终,我们发现ARINA-1介导的细胞内环境氧化还原状态调节导致了纤毛运动的改善,这对MCT有益。我们的研究表明,完整的MCT可减少SARS-CoV-2感染,其药理激活可能作为一种抗COVID-19治疗方法有效。