PB0600 - Circulating platelet-derived extracellular vesicles are increased in severe COVID-19 disease

Monday, June 26, 2023

18:30 – 19:30 ET

Room: Exhibition

Presenting Author(s)

TH

Tuukka A. Helin, MD, PhD (he/him/his)

Clinical chemistry, Coagulation Laboratory
HUS Diagnostics Center
Helsinki, Uusimaa, Finland

Co-Author(s)

MP

Mari Palviainen

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EV core, Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
Helsinki, Uusimaa, Finland
ML

Marja Lemponen

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HUS Diagnostics Centre, HUSLAB Clinical Chemistry, Helsinki University Hospital
Helsinki, Uusimaa, Finland
KM

Katariina Maaninka

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EV core, Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
Helsinki, Uusimaa, Finland
PS

Pia Siljander

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EV core, Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
Helsinki, Uusimaa, Finland
LJ

Lotta Joutsi-Korhonen

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HUS Diagnostics Centre, HUSLAB Clinical Chemistry, Helsinki University Hospital
Helsinki, Uusimaa, Finland

Background: Coagulation disturbances are major contributor to COVID-19 pathogenicity, but there is limited data on the involvement of extracellular vesicles (EVs) and residual cells (RCs).

Aims: We aimed to study EV contribution to coagulation disturbances in hospitalized COVID-19 patients, using D-dimer as marker of coagulation disturbance severity

Methods: Fifty hospitalized COVID-19 patients and 10 healthy controls were assessed for medium EVs (mEVs, 200-1000 nm) and large EVs/RCs (1000-4000 nm) derived from platelets (CD61+), endothelial cells (CD31+), leukocytes (CD45+) and red blood cells (CD235a+), as well as for phosphatidyl serine exposure (lactadherin+) by high sensitivity flow cytometry. Small EVs (sEVs, 50-200 nm) and their CD41a colocalisation with CD9, CD63, and CD81 were studied with single particle interferometric reflectance imaging sensor (SP-IRIS).

Results: Fifteen patients (30%) with high D-dimer (>1.5 mg/L) were compared to controls, and patients with lower D-dimer (≤1.5 mg/mL). Patients with high D-dimer exhibited the highest number of RCs and sEVs (p < 0.05). Differences were seen in the CD61+, CD45+ and lactadherin+ mEVs between D-dimer groups (p < 0.05). Also CD41+ sEV tetraspanin profiles differed between controls and low D-dimer patients.

Conclusion(s): Platelet activation, reflected by increased CD61+ and lactadherin+ mEV and RC levels associated with coagulation disturbances. Tetraspanin colocalisation in platelet-derived sEVs only discriminated controls from patients without the severe coagulation disturbance. Thus EVs and RCs may be used as possible biomarkers in context with coagulation testing.