Autoantibodies against ACE2 and angiotensin type-1 receptors increase severity of COVID-19.


Journal

Journal of autoimmunity
ISSN: 1095-9157
Titre abrégé: J Autoimmun
Pays: England
ID NLM: 8812164

Informations de publication

Date de publication:
08 2021
Historique:
received: 06 05 2021
revised: 30 05 2021
accepted: 01 06 2021
pubmed: 19 6 2021
medline: 23 7 2021
entrez: 18 6 2021
Statut: ppublish

Résumé

The renin-angiotensin system (RAS) plays a major role in COVID-19. Severity of several inflammation-related diseases has been associated with autoantibodies against RAS, particularly agonistic autoantibodies for angiotensin type-1 receptors (AA-AT1) and autoantibodies against ACE2 (AA-ACE2). Disease severity of COVID-19 patients was defined as mild, moderate or severe following the WHO Clinical Progression Scale and determined at medical discharge. Serum AA-AT1 and AA-ACE2 were measured in COVID-19 patients (n = 119) and non-infected controls (n = 23) using specific solid-phase, sandwich enzyme-linked immunosorbent assays. Serum LIGHT (TNFSF14; tumor necrosis factor ligand superfamily member 14) levels were measured with the corresponding assay kit. At diagnosis, AA-AT1 and AA-ACE2 levels were significantly higher in the COVID-19 group relative to controls, and we observed significant association between disease outcome and serum AA-AT1 and AA-ACE2 levels. Mild disease patients had significantly lower levels of AA-AT1 (p < 0.01) and AA-ACE2 (p < 0.001) than moderate and severe patients. No significant differences were detected between males and females. The increase in autoantibodies was not related to comorbidities potentially affecting COVID-19 severity. There was significant positive correlation between serum levels of AA-AT1 and LIGHT (TNFSF14; r

Identifiants

pubmed: 34144328
pii: S0896-8411(21)00091-3
doi: 10.1016/j.jaut.2021.102683
pmc: PMC8193025
pii:
doi:

Substances chimiques

Autoantibodies 0
Autoantigens 0
Receptor, Angiotensin, Type 1 0
ACE2 protein, human EC 3.4.17.23
Angiotensin-Converting Enzyme 2 EC 3.4.17.23

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

102683

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Ana I Rodriguez-Perez (AI)

Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Spain.

Carmen M Labandeira (CM)

Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain; Hospital Alvaro Cunqueiro, University Hospital Complex, Vigo, Spain.

Maria A Pedrosa (MA)

Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Spain.

Rita Valenzuela (R)

Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Spain.

Juan A Suarez-Quintanilla (JA)

Primary Health-Care Unit Fontiñas, IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.

María Cortes-Ayaso (M)

Emergency Department, University Clinical Hospital of Santiago, Santiago de Compostela, Spain.

Placido Mayán-Conesa (P)

Emergency Department, University Clinical Hospital of Santiago, Santiago de Compostela, Spain.

Jose L Labandeira-Garcia (JL)

Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Spain. Electronic address: joseluis.labandeira@usc.es.

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