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Platelet-leukocyte interactions in COVID-19: Contributions to hypercoagulability, inflammation, and disease severity
Eugenio D Hottz1, Patrícia T Bozza2
1Laboratory of Immunothrombosis Department of Biochemistry Federal University of Juiz de Fora (UFJF) Juiz de Fora MG Brazil.
Insights
Platelet-leukocyte interactions in COVID-19 drive hypercoagulability and inflammation, contributing to severe disease. Understanding these interactions is key for developing new therapies to improve outcomes for patients with coronavirus disease 2019.
Area of Science:
- Hematology
- Immunology
- Infectious Diseases
Background:
- Severe COVID-19 is linked to coagulopathy and thromboembolic events, increasing disease severity and mortality.
- Mechanisms underlying COVID-19-associated hypercoagulability and thromboinflammation are of significant research interest.
Purpose of the Study:
- To review mechanisms of platelet activation and leukocyte interactions in COVID-19.
- To highlight the role of platelet-leukocyte interactions in COVID-19 thromboinflammation and disease severity.
Main Methods:
- Review of recent evidence and data presented at the 2021 ISTH Congress.
- Focus on platelet activation, platelet-monocyte, and platelet-neutrophil interactions in COVID-19.
Main Results:
- Platelet activation and interactions with monocytes and neutrophils in COVID-19 promote thromboinflammation.
- These interactions contribute to tissue factor expression and NETosis, linked to thromboembolic complications and poor outcomes.
Conclusions:
- Platelet-leukocyte interactions significantly contribute to COVID-19 immunoregulation, inflammation, and hypercoagulability.
- Understanding these interactions offers potential therapeutic strategies for improving COVID-19 disease severity and patient outcomes.
Abstract:
A State of the Art lecture titled "Platelet-leukocyte interactions in COVID-19: Contributions to hypercoagulability, inflammation and disease severity" was presented at the International Society for Thrombosis and Hemostasis (ISTH) congress in 2021. Severe coronavirus disease 2019 (COVID-19) has been associated with a high incidence of coagulopathy and thromboembolic events that contributes to disease severity and poor outcomes. Therefore, understanding the mechanisms of COVID-19-associated hypercoagulability and thromboinflammation has gained great interest. Here, we review the mechanisms involved in platelet activation and platelet interactions with leukocytes during COVID-19. We highlight recent evidence that platelet activation, platelet-monocyte, and platelet-neutrophil interactions in COVID-19 support pathological thromboinflammation, including in driving tissue factor expression and NETosis, which have been associated with thromboembolic complication and poor outcomes in critically ill patients. The contributions of platelet-leukocyte interactions to COVID-19 immunoregulation, inflammation, and hypercoagulability, as well as their potential implications in disease severity and therapeutic strategies, will be discussed. Finally, we summarize relevant new data on this topic presented during the 2021 ISTH Congress.
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