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[Preprint]. 2022 Feb 2:2021.01.18.21250041.
doi: 10.1101/2021.01.18.21250041.

Endothelial cell-activating antibodies in COVID-19

Hui Shi, Yu Zuo, Sherwin Navaz, Alyssa Harbaugh, Claire K Hoy, Alex A Gandhi, Gautam Sule, Srilakshmi Yalavarthi, Kelsey Gockman, Jacqueline A Madison, Jintao Wang, Melanie Zuo, Yue Shi, Michael D Maile, Jason S Knight, Yogendra Kanthi

Endothelial cell-activating antibodies in COVID-19

Hui Shi et al. medRxiv. .

Update in

  • Endothelial Cell-Activating Antibodies in COVID-19.
    Shi H, Zuo Y, Navaz S, Harbaugh A, Hoy CK, Gandhi AA, Sule G, Yalavarthi S, Gockman K, Madison JA, Wang J, Zuo M, Shi Y, Maile MD, Knight JS, Kanthi Y. Shi H, et al. Arthritis Rheumatol. 2022 Jul;74(7):1132-1138. doi: 10.1002/art.42094. Epub 2022 May 27. Arthritis Rheumatol. 2022. PMID: 35174669 Free PMC article.

Abstract

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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