The Endothelial Dysfunction and Pyroptosis Might Drive the SARS-CoV-2 Lung Injury to the Systemic Immunothrombosis
Abstract
Objective
Endothelial cells that are close to the alveolar-capillary exchange membranes can be activated by SARS-CoV-2 infection leading to cytokine release and macrophage activation syndrome. This could trigger endothelial dysfunction, pyroptosis, and immunothrombosis, which are the vascular changes commonly referred to as COVID-19 endotheliopathy. Thus, this study aimed to identify tissue biomarkers associated with endothelial activation/dysfunction and the pyroptosis pathway in the lung and myocardial samples of COVID-19 patients and to compare them to pandemic Influenza A virus H1N1 subtype – 2009 and Control cases.
Approach and Results
Post-mortem lung (COVID-19 group=6 cases; H1N1 group=10 cases, and Control group=11 cases) and myocardial samples (COVID-19=2 cases and control=1 case) were analyzed using immunohistochemistry and the following monoclonal primary antibodies: anti-CD163, anti-interleukin-6 (IL-6), anti-tumor necrosis factor-alpha (TNF-alpha), anti-intercellular adhesion molecule-1 (ICAM-1), and anti-caspase-1. From the result, IL-6, TNF-alpha, ICAM-1, and caspase-1 showed higher tissue expression in the COVID-19 group than in the H1N1 and control groups.
Conclusion
Our results demonstrated the presence of endotheliopathy and suggest the participation of the pyroptosis pathway in both the pulmonary and myocardial samples. These conditions might lead to systemic immunothrombotic events that could impair the efforts of clinical staff to avoid fatal outcomes. One of the goals of health professionals should be to identify the high-risk of immunothrombosis patients early to block endotheliopathy and its consequences.
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