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Updated: Nov 19, 2025
Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Endothelial cell-activating antibodies in COVID-19
Insights
COVID-19 patients' serum activates endothelial cells, mediated by autoantibodies. These findings highlight a potential mechanism for COVID-19-associated thrombo-inflammation.
Area of Science:
- Immunology
- Vascular Biology
- Infectious Diseases
Background:
- Endothelial dysfunction is a key feature of severe COVID-19, contributing to thrombo-inflammatory complications.
- The specific factors driving this endotheliopathy in COVID-19 remain largely unknown.
Approach:
- Human endothelial cells were exposed to serum/plasma from COVID-19 and sepsis patients.
- Expression of cell adhesion molecules (E-selectin, VCAM-1, ICAM-1) was measured.
- The role of antiphospholipid antibodies and IgG was investigated.
Key Points:
- COVID-19 serum significantly increased endothelial cell adhesion molecule expression.
- Elevated soluble ICAM-1 and E-selectin correlated with disease severity.
- Antiphospholipid antibodies in COVID-19 serum were strongly associated with endothelial activation.
- IgG from COVID-19 patients induced endothelial activation in control serum.
Conclusions:
- This study identifies specific antibodies in some COVID-19 patients that drive endotheliopathy.
- These autoantibodies contribute to the thrombo-inflammatory state observed in severe COVID-19.
- Understanding these antibody-mediated effects provides crucial context for COVID-19 pathogenesis.
Objective:
While endothelial dysfunction has been implicated in the widespread thrombo-inflammatory complications of coronavirus disease-19 ( COVID-19 ), the upstream mediators of endotheliopathy remain for the most part 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 serum or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Cell adhesion molecules (E-selectin, VCAM-1, and ICAM-1) were quantified by in-cell ELISA.
Results:
Serum and plasma from patients with COVID-19 increased surface expression of cell adhesion molecules. Furthermore, levels of soluble ICAM-1 and E-selectin were elevated in patient serum and tracked with disease severity. 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 serum 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.
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