Extracellular vesicles are a late marker of inflammation, hypercoagulability and COVID-19 severity.

Autor:	Barion BG; Universidade de Sao Paulo (USP), Sao Paulo, Brazil., Rocha TRFD; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Ho YL; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Mazetto Fonseca BM; Hematology and Hemotherapy Center of the University of Campinas (UNICAMP), Campinas, Brazil., Okazaki E; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Rothschild C; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Stefanello B; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Rocha VG; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Villaça PR; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil., Orsi FA; Hospital das Clínicas da Faculdade de Medicina da Universidade de São (HCFMUSP), Sao Paulo, Brazil; Department of Pathology, School of Medical Sciences, Universidade de Campinas (UNICAMP), Campinas, Brazil. Electronic address: ferorsi@unicamp.br.
Jazyk:	angličtina
Zdroj:	Hematology, transfusion and cell therapy [Hematol Transfus Cell Ther] 2024 Apr-Jun; Vol. 46 (2), pp. 176-185. Date of Electronic Publication: 2024 Feb 01.
DOI:	10.1016/j.htct.2023.12.003
Abstrakt:	Exacerbated inflammation and coagulation are a hallmark of COVID-19 severity. Extracellular vesicles (EVs) are intercellular transmitters involved in inflammatory conditions, which are capable of triggering prothrombotic mechanisms. Since the release of EVs is potentially associated with COVID-19-induced coagulopathy, the aim of this study was to evaluate changes in inflammation- and hypercoagulability-related EVs during the first month after symptom onset and to determine whether they are associated with disease severity. Blood samples of patients with mild or severe forms of the disease were collected on three occasions: in the second, third and fourth weeks after symptom onset for the quantification by flow cytometry of CD41A (platelet glycoprotein IIb/IIIa), CD162 (PSGL-1), CD31 (PECAM-1) and CD142 cells (tissue factor). Analysis of variance (ANOVA) with repeated measures, Kruskal-Wallis and correlation tests were used. Eighty-five patients were enrolled, 71% of whom had mild disease. Seventeen uninfected individuals served as controls. Compared to controls, both mild and severe COVID-19 were associated with higher EV-CD31 + , EV-CD41 + and EV-CD142 + levels. All EV levels were higher in severe than in mild COVID-19 only after the third week from symptom onset, as opposed to C-reactive protein and D-dimer levels, which were higher in severe than in mild COVID-19 earlier during disease progression. EV levels were also associated with C-reactive protein and D-dimer levels only after the third week of symptoms. In conclusion, EVs expressing CD41A, CD31, TF, and CD162 appear as late markers of COVID-19 severity. This finding may contribute to the understanding of the pathogenesis of acute and possibly long COVID-19. Competing Interests: Conflicts of interest The authors declare they have no conflicts of interest. (Copyright © 2024 Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular. Published by Elsevier España, S.L.U. All rights reserved.)
Databáze:	MEDLINE
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