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Resolvin E1-Chemerin receptor 1 axis is dysregulated in critical COVID-19 patients

2025-10-12Artigo científico Acesso aberto
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dc.contributor.authorSilva-Pereira, Carolina
dc.contributor.authorReina-Couto, Marta
dc.contributor.authorPereira-Terra, Patrícia
dc.contributor.authorTeixeira-Santos, Luísa
dc.contributor.authorMartins, Sandra
dc.contributor.authorPinho, Dora
dc.contributor.authorSoares, Miguel Luz
dc.contributor.authorDias, Cláudia Camila
dc.contributor.authorSarmento, António
dc.contributor.authorTavares, Margarida
dc.contributor.authorGuimarães, João Tiago
dc.contributor.authorPaiva, José-Artur
dc.contributor.authorFraga, Sónia
dc.contributor.authorAlbino-Teixeira, António
dc.contributor.authorRoncon-Albuquerque, Roberto
dc.contributor.authorSousa, Teresa
dc.date.accessioned2026-02-03T15:03:39Z
dc.date.available2026-02-03T15:03:39Z
dc.date.issued2025-10-12
dc.description.abstractResolvin E1 (RvE1) and Resolvin D1 (RvD1) are key resolvins implicated in inflammation resolution of respiratory and infectious diseases. In contrast to cytokines, they have been scarcely explored in COVID-19 and their ability for discriminating COVID-19 severity and patient outcomes has not been compared with that of cytokines. Therefore, among a panel comprising cytokines (interleukin (IL)-1beta, IL-6, IL-10, tumor necrosis factor alpha, interferon gamma and granulocyte-macrophage colony-stimulating factor), RvD1 and RvE1 and their respective receptors (FPR2, Chemerin1), we evaluated which mediators better distinguished COVID-19 severity, the need of mechanical ventilation and patient mortality. Blood was collected from 61 patients with “severe” (n = 27), “critical” (n = 17) and “critical on veno-venous extracorporeal membrane oxygenation (VV-ECMO)” (n = 17) COVID-19 at admission, days 3–4 and days 5–8, and from controls (n = 23) at a single time point. We measured cytokines by multiplex immunoassays, resolvins by enzyme-linked immunosorbent assays, and FPR2 and Chemerin1 mRNA by real-time quantitative polymerase chain reaction. We obtained principal component analysis (PCA)/partial least squares discriminant analysis (PLS-DA) models significantly differentiating (P < 0.001): controls from each patient group; “severe” from all critical patients; patients without or with mechanical ventilation, and survivors from non-survivors. RvE1 consistently showed a variable importance in projection (VIP) score > 2.5 and a p(corr) >0.8, being the most relevant discriminating variable. Univariate and repeated measures multivariate analyses showed higher RvE1 in “critical on VV-ECMO”, mechanically ventilated patients and non-survivors, while Chemerin1 exhibited an opposite profile. RvE1 positively correlated with inflammation and partial pressure of CO2, whereas Chemerin1 correlated with lower inflammation, better respiratory function and lower hospital length of stay. We conclude that RvE1 was the mediator best distinguishing COVID-19 severity and that RvE1-Chemerin1 axis is dysregulated in this disease.eng
dc.description.abstractHighlights: -Serum RvE1 distinguishes COVID-19 severity better than proinflammatory cytokines. -Critical on VV-ECMO COVID-19 patients have higher serum RvE1 and lower Chemerin1 mRNA. -Mechanically ventilated patients have higher serum RvE1 and lower Chemerin1 mRNA. -COVID-19 mortality is associated with higher serum RvE1 and lower Chemerin1 mRNA. -Serum RvE1 and Chemerin1 mRNA correlate with lung function in COVID-19 patients.eng
dc.description.sponsorshipThis work was supported by a RESEARCH 4 COVID-19 grant [project 519, reference number: 613690173] from FCT – Fundação para a Ciência e a Tecnologia (special support for rapid implementation projects for innovative response solutions to COVID-19 pandemic). C. Silva-Pereira is a recipient of a Ph.D. fellowship from FCT and MedInUP [doi:10.54499/UI/BD/150816/2020]. P. Pereira-Terra was supported by a research contract within the scope of the RIFF-HEART project funded by FEDER via COMPETE, Portugal 2020 – Operational Programme for Competitiveness and Internationalization (POCI) [POCI-01-0145-FEDER-032188] and by FCT [PTDC/MEC-CAR/32188/2017].
dc.identifier.citationInt Immunopharmacol. 2025 Dec 10:167:115669. doi: 10.1016/j.intimp.2025.115669. Epub 2025 Oct 12
dc.identifier.doi10.1016/j.intimp.2025.115669
dc.identifier.eissn1878-1705
dc.identifier.issn1567-5769
dc.identifier.pmid41082839
dc.identifier.urihttp://hdl.handle.net/10400.18/10796
dc.language.isoeng
dc.peerreviewedyes
dc.publisherElsevier
dc.relation613690173
dc.relationUI/BD/150816/2020
dc.relationPTDC/MEC-CAR/32188/2017
dc.relation.hasversionhttps://www.sciencedirect.com/science/article/pii/S1567576925016601?via%3Dihub
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCOVID-19
dc.subjectChemerin Receptor 1
dc.subjectCytokines
dc.subjectInflammation Resolution
dc.subjectResolvin E1
dc.subjectVV-ECMO
dc.subjectResolvin E1-Chemerin
dc.titleResolvin E1-Chemerin receptor 1 axis is dysregulated in critical COVID-19 patientseng
dc.typejournal article
dcterms.referenceshttps://ars.els-cdn.com/content/image/1-s2.0-S1567576925016601-mmc1.docx
dspace.entity.typePublication
oaire.citation.startPage115669
oaire.citation.titleInternational Immunopharmacology
oaire.citation.volume167
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85

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