Mucociliary Clearance Augmenting Drugs Block SARS-Cov-2 Replication in Human Airway Epithelial Cells.
Javier Campos-GómezCourtney Fernandez PettyMarina MazurLiping TangGeorge M SolomonReny JosephQian LiJacelyn E Peabody LeverShah Saddad HussainKevin HarrodEzinwanne OnuohaHarrison KimSteven M RowePublished in: bioRxiv : the preprint server for biology (2023)
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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- respiratory tract
- human health
- endothelial cells
- risk assessment
- immune response
- induced apoptosis
- poor prognosis
- metabolic syndrome
- climate change
- cell proliferation
- pluripotent stem cells
- cell death
- dna methylation
- endoplasmic reticulum stress
- adipose tissue
- cell cycle arrest
- signaling pathway
- gene expression
- skeletal muscle
- insulin resistance
- combination therapy
- replacement therapy