The Endothelial Dysfunction and Pyroptosis Driving the SARS-CoV-2 Immune-Thrombosis

Objective: Endothelial activation after viral infection could contribute to changes in the vascular glycocalyx associated with programmed inflammatory cell death called pyroptosis. Thus, our goal is to recognize endothelial activation and pyroptosis in lung and myocardial samples of Coronavirus disease (COVID-19) cases and compare to H1N1pdm09 and control cases. Approach and Results: Post-mortem lung (6 cases of COVID-19 group; 10 cases of H1N1 group and 11 cases of Control group) and myocardial samples (2 cases of COVID-19 and one control) were analyzed by conventional immunohistochemistry by using antibodies to identify molecules involving with endothelial activation (CD163, Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-alpha), Intercellular Adhesion Molecule 1 (ICAM-1)) and pyroptosis (Caspase-1). As a result, IL-6, TNF-alpha, ICAM-1, and Caspase-1 show higher tissue expression in the COVID-19 group compared to H1N1 and Control groups. Conclusion: Our results indicate that the vascular endothelium has been activated and the presence of pyroptosis and endothelial dysfunction in lung and myocardial samples. These conditions could lead to a systemic immune-thrombotic process that may impair the clinical staff9s efforts to prevent fatal outcomes. One aim of the health professionals is to avoid COVID-19 systemic vascular injury and immune-thrombosis by blocking the endothelial dysfunction and its consequences.