ArticleFrontiers in immunology2023
Circulating extracellular particles from severe COVID-19 patients show altered profiling and innate lymphoid cell-modulating ability.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 10 citations in OpenAlex.
- Multi-parametric profiling of plasma-derived extracellular vesicles reveals a disease-associated molecular signature supporting a liquid biopsy approach in myelofibrosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Evaluating Novel Direct Injection Liquid Chromatography-Mass Spectrometry Method and Extraction-Based Workflows for Untargeted Lipidomics of Extracellular Vesicles.Journal of proteome research · 2025Article
- Extracellular Vesicles Alter Trophoblast Function in Pregnancies Complicated by COVID-19.Journal of extracellular vesicles · 2025Article
- Novel Immune biomarkers for the early stratification of oligoarthritis patients at risk of developing polyarticular extension.Frontiers in immunology · 2025Article
- ILC2-mediated immune crosstalk in chronic (vascular) inflammation.Frontiers in immunology · 2023Review
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Authors and funding
21 authors at 6 institutions in 2 countries.
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Abstract
Introduction: Extracellular vesicles (EVs) and particles (EPs) represent reliable biomarkers for disease detection. Their role in the inflammatory microenvironment of severe COVID-19 patients is not well determined. Here, we characterized the immunophenotype, the lipidomic cargo and the functional activity of circulating EPs from severe COVID-19 patients (Co-19-EPs) and healthy controls (HC-EPs) correlating the data with the clinical parameters including the partial pressure of oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) and the sequential organ failure assessment (SOFA) score. Methods: Peripheral blood (PB) was collected from COVID-19 patients (n=10) and HC (n=10). EPs were purified from platelet-poor plasma by size exclusion chromatography (SEC) and ultrafiltration. Plasma cytokines and EPs were characterized by multiplex bead-based assay. Quantitative lipidomic profiling of EPs was performed by liquid chromatography/mass spectrometry combined with quadrupole time-of-flight (LC/MS Q-TOF). Innate lymphoid cells (ILC) were characterized by flow cytometry after co-cultures with HC-EPs or Co-19-EPs. Results: We observed that EPs from severe COVID-19 patients: 1) display an altered surface signature as assessed by multiplex protein analysis; 2) are characterized by distinct lipidomic profiling; 3) show correlations between lipidomic profiling and disease aggressiveness scores; 4) fail to dampen type 2 innate lymphoid cells (ILC2) cytokine secretion. As a consequence, ILC2 from severe COVID-19 patients show a more activated phenotype due to the presence of Co-19-EPs. Discussion: In summary, these data highlight that abnormal circulating EPs promote ILC2-driven inflammatory signals in severe COVID-19 patients and support further exploration to unravel the role of EPs (and EVs) in COVID-19 pathogenesis.
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