Sepideh Zununi Vahed
1 
, Shahram Ghiyasvand
1, Seyed Mahdi Hosseiniyan Khatibi
1 , Bhargav Patel
2 , Mohammadali Mohajel Shoja
3, Ramin Tolouian
4 , Mohammadreza Ardalan
1 1 Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
2 Department of Internal Medicine, University of Arizona, Tucson, AZ, USA
3 Department of Surgery, University of Illinois at Chicago-Metropolitan Group Hospitals (UIC-MGH), Chicago, Illinois, USA
4 Division of Nephrology, College of Medicine, University of Arizona, Tucson, AZ, USA
Abstract
SARS-CoV-2 is a worldwide pandemic, that has led to the morbidity and mortality of millions of people. This virus rapidly proliferates and destroys lung epithelial cells directly, which is worsened by a subsequent cytokine storm. This cytokine storm diffusely damages the alveolar barriers and leads to fibrin and fluid exudation, hyaline membrane formation, and infiltration of inflammatory cells into the lung causing acute respiratory distress syndrome (ARDS). To date, there exists no medication to treat SARS-CoV-2 infection and novel new therapeutics are still being explored to prevent or limit the damage to the lung. Sphingosine 1-phosphate (S1P) is an effective bioactive lipid mediator and its related signaling pathways are vital for endothelial cell integrity. Stabilizing the pulmonary endothelial barrier and decreasing the inflammatory infiltrate by S1P analogs such as Fingolimod (FTY720-P) would be a new therapeutic approach for the hindrance of pulmonary exudation and subsequent ARDS.