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Early SARS-CoV-2 infection: Platelet-neutrophil complexes and platelet function
Marina Rieder1,2, Niklas Baldus1,2, Daniela Stallmann2
1Interdisciplinary Medical Intensive Care, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Insights
COVID-19 patients show impaired platelet aggregation and responsiveness, despite no signs of platelet preactivation. However, increased platelet-neutrophil complexes suggest early cellular interactions occur in moderate COVID-19.
Area of Science:
- Hematology
- Immunology
- Infectious Diseases
Background:
- Conflicting reports exist on platelet activity in COVID-19 patients.
- Platelet dysfunction may contribute to thromboembolic complications in COVID-19.
Purpose of the Study:
- To evaluate platelet reactivity in patients with moderate COVID-19 at early disease stages.
- To investigate platelet activation and interactions with neutrophils in COVID-19.
Main Methods:
- Prospective analysis of 20 COVID-19 patients, 55 SARS-CoV-2-negative controls, and 15 healthy subjects.
- Assessed platelet reactivity using aggregometry and flow cytometry.
- Analyzed platelet-neutrophil complexes and neutrophil adhesion receptor expression.
Main Results:
- COVID-19 patients exhibited significantly impaired platelet aggregation and GPIIb/IIIa activation.
- No evidence of in vivo platelet preactivation or exhaustion was observed.
- Elevated circulating platelet-neutrophil complexes were found in COVID-19 patients.
- Upregulation of CD11b and CD66b on neutrophils was noted in COVID-19 patients.
Conclusions:
- Early-stage moderate COVID-19 is characterized by reduced platelet responsiveness but increased platelet-neutrophil complexes.
- Platelet-neutrophil interactions may occur in COVID-19 independently of prior platelet activation.
Background:
Conflicting results have been reported on platelet activity ex vivo and responsiveness in vitro among patients with COVID-19 with or without thromboembolic complications.
Objectives:
To assess platelet reactivity in patients with moderate disease at early stages of COVID-19.
Methods:
We performed a prospective, descriptive analysis of 100 consecutive patients presenting with suspected SARS-CoV-2 infection at University Medical Center Freiburg during the first or second wave of the pandemic. Following polymerase chain reaction testing and compliance with study inclusion criteria, 20 SARS-CoV-2-positive and 55 SARS-CoV-2-negative patients (serving as patient controls) were enrolled. In addition, 15 healthy subjects were included. Platelet reactivity was assessed using whole-blood impedance aggregometry and flow cytometry in response to various agonists.
Results:
Platelet aggregation was significantly impaired in the patients with COVID-19 compared with that in the patient controls or healthy subjects. The reduced platelet responsiveness in the patients with COVID-19 was associated with impaired activation of GPIIb/IIIa (αIIbβ3). In contrast, low expression of P-selectin at baseline and intact secretion upon stimulation in vitro suggest that no preactivation in vivo, leading to "exhausted" platelets, had occurred. The proportion of circulating platelet-neutrophil complexes was significantly higher in the patients with COVID-19 (mean ± SD, 41% ± 13%) than in the patient controls (18% ± 7%; 95% CI, 11.1-34.1; P = .0002) or healthy subjects (17% ± 4%; 95% CI, 13.8-33.8; P < .0001). An analysis of neutrophil adhesion receptors revealed upregulation of CD11b (α-subunit of αMβ2) and CD66b (CEACAM8) but not of CD162 (PSGL-1) in the patients with COVID-19.
Conclusion:
Despite reduced platelet responsiveness, platelet-neutrophil complexes are increased at early stages of moderate disease. Thus, this cellular interaction may occur during COVID-19 without preceding platelet activation.
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