Circulating extracellular vesicles are endowed with enhanced procoagulant activity in SARS-CoV-2 infection.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
May 2021
Historique:
received: 18 01 2021
revised: 26 03 2021
accepted: 14 04 2021
pubmed: 11 5 2021
medline: 9 6 2021
entrez: 10 5 2021
Statut: ppublish

Résumé

Coronavirus-2 (SARS-CoV-2) infection causes an acute respiratory syndrome accompanied by multi-organ damage that implicates a prothrombotic state leading to widespread microvascular clots. The causes of such coagulation abnormalities are unknown. The receptor tissue factor, also known as CD142, is often associated with cell-released extracellular vesicles (EV). In this study, we aimed to characterize surface antigens profile of circulating EV in COVID-19 patients and their potential implication as procoagulant agents. We analyzed serum-derived EV from 67 participants who underwent nasopharyngeal swabs molecular test for suspected SARS-CoV-2 infection (34 positives and 33 negatives) and from 16 healthy controls (HC), as referral. A sub-analysis was performed on subjects who developed pneumonia (n = 28). Serum-derived EV were characterized for their surface antigen profile and tested for their procoagulant activity. A validation experiment was performed pre-treating EV with anti-CD142 antibody or with recombinant FVIIa. Serum TNF-α levels were measured by ELISA. Profiling of EV antigens revealed a surface marker signature that defines circulating EV in COVID-19. A combination of seven surface molecules (CD49e, CD209, CD86, CD133/1, CD69, CD142, and CD20) clustered COVID (+) versus COVID (-) patients and HC. CD142 showed the highest discriminating performance at both multivariate models and ROC curve analysis. Noteworthy, we found that CD142 exposed onto surface of EV was biologically active. CD142 activity was higher in COVID (+) patients and correlated with TNF-α serum levels. In SARS-CoV-2 infection the systemic inflammatory response results in cell-release of substantial amounts of procoagulant EV that may act as clotting initiation agents, contributing to disease severity. Cardiocentro Ticino Institute, Ente ospedaliero Cantonale, Lugano-Switzerland.

Sections du résumé

BACKGROUND BACKGROUND
Coronavirus-2 (SARS-CoV-2) infection causes an acute respiratory syndrome accompanied by multi-organ damage that implicates a prothrombotic state leading to widespread microvascular clots. The causes of such coagulation abnormalities are unknown. The receptor tissue factor, also known as CD142, is often associated with cell-released extracellular vesicles (EV). In this study, we aimed to characterize surface antigens profile of circulating EV in COVID-19 patients and their potential implication as procoagulant agents.
METHODS METHODS
We analyzed serum-derived EV from 67 participants who underwent nasopharyngeal swabs molecular test for suspected SARS-CoV-2 infection (34 positives and 33 negatives) and from 16 healthy controls (HC), as referral. A sub-analysis was performed on subjects who developed pneumonia (n = 28). Serum-derived EV were characterized for their surface antigen profile and tested for their procoagulant activity. A validation experiment was performed pre-treating EV with anti-CD142 antibody or with recombinant FVIIa. Serum TNF-α levels were measured by ELISA.
FINDINGS RESULTS
Profiling of EV antigens revealed a surface marker signature that defines circulating EV in COVID-19. A combination of seven surface molecules (CD49e, CD209, CD86, CD133/1, CD69, CD142, and CD20) clustered COVID (+) versus COVID (-) patients and HC. CD142 showed the highest discriminating performance at both multivariate models and ROC curve analysis. Noteworthy, we found that CD142 exposed onto surface of EV was biologically active. CD142 activity was higher in COVID (+) patients and correlated with TNF-α serum levels.
INTERPRETATION CONCLUSIONS
In SARS-CoV-2 infection the systemic inflammatory response results in cell-release of substantial amounts of procoagulant EV that may act as clotting initiation agents, contributing to disease severity.
FUNDING BACKGROUND
Cardiocentro Ticino Institute, Ente ospedaliero Cantonale, Lugano-Switzerland.

Identifiants

pubmed: 33971404
pii: S2352-3964(21)00162-6
doi: 10.1016/j.ebiom.2021.103369
pmc: PMC8104913
pii:
doi:

Substances chimiques

Antigens, Surface 0
Biomarkers 0
TNF protein, human 0
Tumor Necrosis Factor-alpha 0
Thromboplastin 9035-58-9

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103369

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest Authors have nothing to disclose.

Auteurs

Carolina Balbi (C)

Laboratory of Cellular and Molecular Cardiology, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale, Lugano, Switzerland; Center for Molecular Cardiology, Zurich, Switzerland.

Jacopo Burrello (J)

Laboratory for Cardiovascular Theranostics, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale Lugano, Switzerland.

Sara Bolis (S)

Laboratory of Cellular and Molecular Cardiology, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale, Lugano, Switzerland; Laboratory for Cardiovascular Theranostics, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale Lugano, Switzerland.

Edoardo Lazzarini (E)

Laboratory for Cardiovascular Theranostics, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale Lugano, Switzerland.

Vanessa Biemmi (V)

Laboratory for Cardiovascular Theranostics, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale Lugano, Switzerland.

Enea Pianezzi (E)

Laboratory of Microbiology, Ente Ospedaliero Cantonale, Bellinzona, Switzerland.

Alessio Burrello (A)

Department of Electrical, Electronic and Information Engineering (DEI), University of Bologna, Bologna, Italy.

Elena Caporali (E)

Cardiology Department, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale, Lugano, Switzerland.

Lorenzo Gauthier Grazioli (LG)

Internal Medicine Department, Ospedale Regionale di Lugano, Ente Ospedaliero Cantonale, Lugano, Switzerland.

Gladys Martinetti (G)

Laboratory of Microbiology, Ente Ospedaliero Cantonale, Bellinzona, Switzerland.

Tanja Fusi-Schmidhauser (T)

Internal Medicine Department, Ospedale Regionale di Lugano, Ente Ospedaliero Cantonale, Lugano, Switzerland.

Giuseppe Vassalli (G)

Laboratory of Cellular and Molecular Cardiology, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale, Lugano, Switzerland; Center for Molecular Cardiology, Zurich, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera italiana, Lugano, Switzerland.

Giorgia Melli (G)

Faculty of Biomedical Sciences, Università della Svizzera italiana, Lugano, Switzerland; Laboratory for Biomedical Neurosciences, Neurocenter of Southern Switzerland, Lugano, Switzerland.

Lucio Barile (L)

Laboratory for Cardiovascular Theranostics, Istituto Cardiocentro Ticino, Ente Ospedaliero Cantonale Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera italiana, Lugano, Switzerland; Institute of Life Science, Scuola Superiore Sant'Anna, Pisa, Italy. Electronic address: lucio.barile@cardiocentro.org.

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Classifications MeSH