Abstract
Acute respiratory distress syndrome (ARDS) is the main cause of
morbidity and mortality in Coronavirus disease 19 (Covid-19) for which
as of now there is no effective treatment. ARDS is caused and sustained
by an uncontrolled inflammatory activation characterized by a massive
release of cytokines (cytokine storm), diffuse lung edema, inflammatory
cell infiltraton and disseminated coagulation. Macrophage and T
lymphocyte dysfunction plays a central role in this syndrome. In several
experimental in vitro and in vivo models, many of these
pathophysiological changes are triggered by stimulation of the P2X7
receptor. We hypothesize that this receptor might be an ideal candidate
to target in Covid-19-associated ARDS.