ABSTRACT
Objective
Endothelial dysfunction has been implicated in the widespread thrombo-inflammatory complications of coronavirus disease-19 ( COVID-19 ), although the upstream mediators of endotheliopathy remain cryptic. Our aim was to identify circulating factors contributing to endothelial cell activation and dysfunction in COVID-19.
Methods
Human endothelial cells were cultured in the presence of sera or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Cell adhesion molecules (E-selectin, ICAM-1 and VCAM-1) were quantified by in-cell ELISA.
Results
Sera and plasma from patients with COVID-19, and to a lesser extent from patients with sepsis, increased surface expression of cell adhesion molecules. The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium. Depletion of total IgG from antiphospholipid antibody-positive sera markedly restrained upregulation of cell adhesion molecules. Conversely, supplementation of control serum with patient IgG was sufficient to trigger endothelial activation.
Conclusion
These data are the first to suggest that some patients with COVID-19 have potentially diverse antibodies that drive endotheliopathy, adding important context regarding thrombo-inflammatory effects of autoantibodies in severe COVID-19.
Full Text Availability
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