Endothelial dysfunction in COVID-19: Insights from bronchoalveolar lavage and molecular markers

Endothelium play a crucial role in immune responses and inflammatory reactions. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces an exaggerated immune response. Therefore, in this study the roles of endothelium in the manifestation of sever Coronavirus disease 2019 (COVID-19) was investigated. The direct effects of SARS-CoV-2 alpha (SCA) and SARS-CoV-2 omicron (SCO), on endothelial function were investigated in bronchoalveolar lavage (BAL), that were obtained by leftover samples of Covid-19 patients who were compared to forty control group to enrich genes and proteins expression of Intracellular Adhesion Molecule-1 (ICAM-1), Vascular cell adhesion molecules 1 (VCAM-1), Nuclear factor erythroid 2–related factor 2 (Nrf2), NADPH oxidase 2 (NOX2), von Willebrand factor (vWF) and Inducible nitric oxide synthases (iNOS). SARS-CoV-2 increased gene and protein expression of ICAM-1. SCA and SCO increase VCAM-1 gene expression. VCAM-1 protein expression in SCO increased too. vWF gene expression increased in SCO. vWF protein expressed highly too. SCO group showed a significant increase in iNOS gene expression. Although, NOX2 gene increased by SCA and SCO and its protein increased too, Nrf2 gene and protein decreased by SARS-CoV-2. Based on our findings, severe COVID-19 can cause damage to vascular endothelium, which is crucial in affecting multiple organ dysfunction. Our research indicates that endothelial dysfunction is a significant factor in the progression of severe COVID-19 in comparison to other respiratory diseases.