期刊
ARTHRITIS & RHEUMATOLOGY
卷 -, 期 -, 页码 -出版社
WILEY
DOI: 10.1002/art.42094
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资金
- Rheumatology Research Foundation
- Arthritis National Research Foundation
- VA Healthcare System
- Michigan Medicine Frankel Cardiovascular Center
- A. Alfred Taubman Medical Research Institute
- NIH [R01-HL-115138]
- Burroughs Wellcome Fund
- Lupus Research Alliance
- Intramural Research Program of the National Heart, Lung, and Blood Institute, NIH
- Lasker Foundation
- University of Michigan Frankel Cardiovascular Center
- Falk Medical Research Trust Catalyst Award
This study found that circulating factors in the serum or plasma of COVID-19 patients contribute to endothelial cell activation and dysfunction. Particularly, the presence of circulating antiphospholipid antibodies is closely associated with the ability of COVID-19 serum to activate endothelial cells.
Objective While endothelial dysfunction has been implicated in the widespread thromboinflammatory complications of COVID-19, the upstream mediators of endotheliopathy remain, for the most part, unknown. This study was undertaken 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-19-related sepsis. Cell adhesion molecules (E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 [ICAM-1]) were quantified using in-cell enzyme-linked immunosorbent assay. Results Serum and plasma from COVID-19 patients increased surface expression of cell adhesion molecules. Furthermore, levels of soluble ICAM-1 and E-selectin were elevated in patient serum and correlated 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 reduced the up-regulation 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 indicate that some COVID-19 patients have potentially diverse antibodies that drive endotheliopathy, providing important context regarding thromboinflammatory effects of autoantibodies in severe COVID-19.
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