INTRODUCTION: In late 2019, unusual pneumonia emerged in the city of Wuhan, China, and quickly spread to other parts of the world, being declared a pandemic by the World Health Organization (WHO). The disease was named Coronavirus-2019 (COVID-19), and the causative pathogen was found to be a novel coronavirus named SARS-CoV-2 due to the close equivalence with severe acute syndrome coronavirus (SARS-CoV). MATERIALS AND METHOD: Infection with the new coronavirus causes an inflammatory response that triggers a phenomenon called a cytokine storm, in which excessive production of inflammatory cytokines and chemokines occurs. Excess cytokines induce endothelial dysfunction, leading to acute vascular inflammation and thrombosis. OBJECIVES: In the present study, sera from patients with moderate (n=6), severe (n=6), and patients who died (n=6) were used. Human umbilical vein endothelial cells were incubated for 2 and 24 hours with pooled serum from the groups. After incubation, cells were immunostained with anti-PECAM-1 and anti-CD36 for expression evaluation by flow cytometry. RESULTS: The results of the study showed increased expression of PECAM-1 molecule, an adhesion molecule important for the diapedesis of inflammatory cells, and CD36, a multifunctional glycoprotein that is related to several biological processes, including the inflammatory process and downregulation of angiogenesis. FINAL CONSIDERATIONS: The gradual increase in the expression of both PECAM-1 and CD26 according to the severity of the disease demonstrates that the concentration of inflammatory molecules present in the serum has an influence on endothelial dysfunction.
