Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19
| Autor: | Fernando A. Bozza, Lívia Teixeira, Ester A. Barreto, Eugenio D. Hottz, Cassia Righy, Camila R. R. Pão, Pedro Kurtz, Lohanna Palhinha, Sérgio Franco, Thiago Moreno L. Souza, Patrícia T. Bozza, Isaclaudia G. de Azevedo-Quintanilha |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Adult
Blood Platelets Male 0301 basic medicine P-selectin Pneumonia Viral Immunology 030204 cardiovascular system & hematology Biochemistry Monocytes Thromboplastin Pathogenesis Betacoronavirus 03 medical and health sciences Tissue factor 0302 clinical medicine Abciximab Humans Medicine Platelet Prospective Studies Platelet activation Pandemics SARS-CoV-2 business.industry COVID-19 Cell Biology Hematology Blood Coagulation Disorders Middle Aged Platelet Activation Prognosis Platelets and Thrombopoiesis Survival Rate P-Selectin 030104 developmental biology Coagulation Case-Control Studies Hemostasis Female Coronavirus Infections business Biomarkers Follow-Up Studies medicine.drug |
| Zdroj: | Blood |
| ISSN: | 1528-0020 0006-4971 |
| Popis: | There is a Blood Commentary on this article in this issue. Key Points Increased platelet activation and platelet-monocyte aggregate formation associate with poor outcome in severe COVID-19 patients. Platelets from severe COVID-19 patients induce monocyte TF expression through P-selectin and integrin αIIb/β3 signaling. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emergent pathogen responsible for the coronavirus disease 2019 (COVID-19). Since its emergence, the novel coronavirus has rapidly achieved pandemic proportions causing remarkably increased morbidity and mortality around the world. A hypercoagulability state has been reported as a major pathologic event in COVID-19, and thromboembolic complications listed among life-threatening complications of the disease. Platelets are chief effector cells of hemostasis and pathological thrombosis. However, the participation of platelets in the pathogenesis of COVID-19 remains elusive. This report demonstrates that increased platelet activation and platelet-monocyte aggregate formation are observed in severe COVID-19 patients, but not in patients presenting mild COVID-19 syndrome. In addition, exposure to plasma from severe COVID-19 patients increased the activation of control platelets ex vivo. In our cohort of COVID-19 patients admitted to the intensive care unit, platelet-monocyte interaction was strongly associated with tissue factor (TF) expression by the monocytes. Platelet activation and monocyte TF expression were associated with markers of coagulation exacerbation as fibrinogen and D-dimers, and were increased in patients requiring invasive mechanical ventilation or patients who evolved with in-hospital mortality. Finally, platelets from severe COVID-19 patients were able to induce TF expression ex vivo in monocytes from healthy volunteers, a phenomenon that was inhibited by platelet P-selectin neutralization or integrin αIIb/β3 blocking with the aggregation inhibitor abciximab. Altogether, these data shed light on new pathological mechanisms involving platelet activation and platelet-dependent monocyte TF expression, which were associated with COVID-19 severity and mortality. Visual Abstract |
| Databáze: | OpenAIRE |
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