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Complement activation and endothelial perturbation parallel COVID-19 severity and activity.

Massimo Cugno¹, Pier Luigi Meroni², Roberta Gualtierotti¹

¹Università degli Studi di Milano, Department of Pathophysiology and Transplantation, Milan, Italy; Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Internal Medicine and Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Milan, Italy.

Journal of Autoimmunity

|November 3, 2020

Summary

Complement activation is elevated in severe COVID-19, correlating with endothelial damage and disease severity. Levels decrease during remission, suggesting complement plays a role in COVID-19 pathophysiology and could be a therapeutic target.

Keywords:

C5a COVID-19 Complement Endothelium SC5b-9 von Willebrand factor

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On-Chip Endothelial Inflammatory Phenotyping

On-Chip Endothelial Inflammatory Phenotyping

Published on: July 21, 2012

Area of Science:

Immunology
Pathophysiology
Vascular Biology

Background:

Emerging evidence suggests the complement system's involvement in severe COVID-19 manifestations.
The specific contribution of complement to COVID-19-associated endotheliopathy and hypercoagulability remains unclear.

Purpose of the Study:

To investigate the association between complement activation, endothelial damage, and disease severity in COVID-19 patients.

Main Methods:

A cohort of 148 COVID-19 patients was assessed for complement activation markers (SC5b-9, C5a) and endothelial perturbation markers (vWF, t-PA, PAI-1, sTM, sE-selectin).
Measurements were taken at hospital admission and 30 days later.

Main Results:

Patients exhibited elevated plasma levels of SC5b-9, C5a, vWF, t-PA, and PAI-1.
SC5b-9 levels positively correlated with vWF and disease severity.
Significantly increased sE-selectin levels were observed only in severe COVID-19 cases.
Follow-up at 30 days showed significant reductions in SC5b-9, C5a, and vWF levels.

Conclusions:

Complement activation intensifies during COVID-19 progression and decreases during remission, highlighting its role in disease pathophysiology.
The link between complement activation and endothelial damage markers suggests complement's contribution to tissue injury.
Targeting the complement system may offer a potential therapeutic strategy for COVID-19.