Journal Article Epublish 2 citations
PubMed: 37509430 DOI: 10.3390/biomedicines11071790
Hydrogen Sulfide Ameliorates SARS-CoV-2-Associated Lung Endothelial Barrier Disruption.
Biomedicines 11(7)
Authors: Olivier Escaffre, Peter Szaniszlo, Gabor Törő, Caitlyn L Vilas, Brenna J Servantes, Ernesto Lopez, Terry L Juelich, Corri B Levine, Susan L F McLellan, Jessica C Cardenas, Alexander N Freiberg, Katalin Módis
Affiliations
- Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
- Institute for Human Infections & Immunity, Sealy & Smith Foundation, University of Texas Medical Branch, Galveston, TX 77555, USA.
- Department of Surgery, University of Texas Medical Branch, Galveston, TX 77555, USA.
- John Sealy School of Medicine, University of Texas Medical Branch, Galveston, TX 77555, USA.
- Department of Anesthesiology, University of Texas Medical Branch, Galveston, TX 77555, USA.
- Department of Internal Medicine, Division of Infectious Diseases, University of Texas Medical Branch, Galveston, TX 77555, USA.
- The Center for Translational Injury Research, Department of Surgery, UTHealth McGovern Medical School, Houston, TX 77030, USA.
- The Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, TX 77555, USA.
Abstract
Recent studies have confirmed that lung microvascular endothelial injury plays a critical role in the pathophysiology of COVID-19. Our group and others have demonstrated the beneficial effects of HS in several pathological processes and provided a rationale for considering the therapeutic implications of HS in COVID-19 therapy. Here, we evaluated the effect of the slow-releasing HS donor, GYY4137, on the barrier function of a lung endothelial cell monolayer in vitro, after challenging the cells with plasma samples from COVID-19 patients or inactivated SARS-CoV-2 virus. We also assessed how the cytokine/chemokine profile of patients' plasma, endothelial barrier permeability, and disease severity correlated with each other. Alterations in barrier permeability after treatments with patient plasma, inactivated virus, and GYY4137 were monitored and assessed by electrical impedance measurements in real time. We present evidence that GYY4137 treatment reduced endothelial barrier permeability after plasma challenge and completely reversed the endothelial barrier disruption caused by inactivated SARS-CoV-2 virus. We also showed that disease severity correlated with the cytokine/chemokine profile of the plasma but not with barrier permeability changes in our assay. Overall, these data demonstrate that treatment with HS-releasing compounds has the potential to ameliorate SARS-CoV-2-associated lung endothelial barrier disruption.
MeSH
Plasma, Cells, Therapeutics, Sulfides, Lung, Sars Virus, Covid-19, Sars-Cov-2