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.
Highlights
Severe acute respiratory syndrome coronavirus virus 2 (SARS-CoV-2) targets the respiratory epithelial cells, which leads to a severe respiratory presentation in 15% to 20% of patients
Sphingosine 1-phosphate (S1P) binds to a five-membrane related G-protein coupled receptors (GPCRs) including S1PR 1, -2, and -3 which are present in the cardiovascular system, while
The important findings were prominent lymphocytic interstitial infiltration dominated by cytotoxic CD8 and Th17 cells. These findings show the importance of inflammatory cells in lethal cases of SARS-CoV-2 infection [6]
Summary
Sphingosine 1 phosphate agonists (SPI); a potential agent to prevent acute lung injury in COVID-19.
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