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Abstract Number: 0075

Endothelial Cell-activating Antibodies in COVID-19

Hui Shi1, Yu Zuo2, Sherwin Navaz2, Alyssa Harbaugh2, Claire Hoy2, Alex Gandhi2, Gautam Sule2, Srilakshmi Yalavarthi2, Kelsey Gockman2, Jacqueline Madison2, Jintao Wang2, Melanie zuo2, Yue Shi3, Michael Maile2, Yogendra Kanthi2 and Jason Knight2, 1Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 2University of Michigan, Ann Arbor, MI, 3Shanghai Sports School, Shanghai, China (People's Republic)

Meeting: ACR Convergence 2021

Keywords: antiphospholipid syndrome, Autoantibody(ies), cell adhension, COVID-19, endothelial cells

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Session Information

Date: Saturday, November 6, 2021

Title: Antiphospholipid Syndrome Poster (0069–0083)

Session Type: Poster Session A

Session Time: 8:30AM-10:30AM

Background/Purpose: Patients with COVID-19 are at high risk for occlusion of vascular beds of all sizes. Considering endothelial cell activation has regularly been described as part of the COVID-19 thrombo-inflammatory storm, we aimed to characterize potential upstream mediators of this activation including neutrophil extracellular traps (NETs) and antiphospholipid antibodies (aPL).

Methods: Cultured human umbilical vein endothelial cells (HUVECs) were exposed to sera from 118 patients hospitalized with COVID-19. Plasma samples from 100 non-COVID sepsis patients were also characterized alongside 72 COVID samples. Upregulation of surface cell adhesion molecules E-selectin, ICAM-1, and VCAM-1 was determined by in-cell ELISA. Soluble E-selectin was measured in serum. HUVECs were also stimulated with IgG purified from three COVID patients positive for anticardiolipin IgG and separately five positive for anti-PS/PT IgG.

Results: As compared with sera from 38 healthy controls, COVID sera triggered an activated HUVEC phenotype as evidenced by markedly increased surface expression of the cell adhesion molecules E-selectin (mean 1.67-fold increase, p< 0.0001), VCAM-1 (mean 1.89-fold increase, p< 0.0001), and ICAM-1 (mean 1.66-fold increase, p< 0.0001). While non-COVID sepsis plasma elicited higher expression of surface ICAM-1 than did control plasma, the effect was even more robust with COVID-19 plasma (p< 0.05 comparing COVID-19 to sepsis). Beyond the in-cell ELISA platform, we also found significantly higher levels of soluble E-selectin in COVID serum as compared with healthy controls (p< 0.0001), where it correlated with clinical parameters that track with COVID-19 severity including C-reactive protein (r=0.31, p=0.005), D-dimer (r=0.31, p=0.008), calprotectin (r=0.29, p=0.003), and oxygenation efficiency (r=-0.31, p=0.002). One marker of NET remnants, myeloperoxidase-DNA complexes, modestly correlated with the ability of serum to increase expression of both VCAM-1 (r=0.26, p< 0.01) and ICAM-1 (r=0.28, p< 0.01) on HUVECs, while cell-free DNA and citrullinated histone H3 (additional markers of NETs) correlated with VCAM-1 only (r=0.24, p< 0.05 and r=0.22, p< 0.05, respectively). Interestingly, we detected robust correlations between various aPL in serum, especially anticardiolipin IgG/M and anti-phosphatidlyserine/prothrombin (anti-PS/PT) IgG/M, and the three markers of HUVEC activation (E-selectin, VCAM-1, and ICAM-1) (Table 1). As compared with mock depletion, IgG depletion strongly abrogated the ability of pooled COVID sera (anticardiolipin-positive and anti-PS/PT-positive) to upregulate HUVEC E-selectin (p< 0.01 and p< 0.05, respectively), VCAM-1 (p< 0.05 and p< 0.01) and ICAM-1 (p< 0.01 for both). Furthermore, IgG (100 μg/ml) purified from the anticardiolipin-positive and anti-PS/PT-positive COVID serum increased expression of ICAM-1 (p< 0.01 for both) when spiked into control serum.

Conclusion: These data are the first to suggest that patient antibodies are a driver of endothelial cell activation in COVID-19 and add important context regarding thrombo-inflammatory effects of aPL-like autoantibodies in severe COVID-19.


Disclosures: H. Shi, None; Y. Zuo, None; S. Navaz, None; A. Harbaugh, None; C. Hoy, None; A. Gandhi, None; G. Sule, None; S. Yalavarthi, None; K. Gockman, None; J. Madison, None; J. Wang, None; M. zuo, None; Y. Shi, None; M. Maile, None; Y. Kanthi, None; J. Knight, None.

To cite this abstract in AMA style:

Shi H, Zuo Y, Navaz S, Harbaugh A, Hoy C, Gandhi A, Sule G, Yalavarthi S, Gockman K, Madison J, Wang J, zuo M, Shi Y, Maile M, Kanthi Y, Knight J. Endothelial Cell-activating Antibodies in COVID-19 [abstract]. Arthritis Rheumatol. 2021; 73 (suppl 9). https://acrabstracts.org/abstract/endothelial-cell-activating-antibodies-in-covid-19/. Accessed .
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