Neutrophil extracellular traps and thrombosis in COVID-19
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Neutrophil extracellular traps and thrombosis in COVID‑19 Yu Zuo1 · Melanie Zuo2 · Srilakshmi Yalavarthi1 · Kelsey Gockman1 · Jacqueline A. Madison1 · Hui Shi1,3 · Wrenn Woodard4 · Sean P. Lezak4 · Njira L. Lugogo5 · Jason S. Knight1 · Yogendra Kanthi6,7 Accepted: 26 October 2020 © This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2020
Abstract Studies of patients with COVID-19 have demonstrated markedly dysregulated coagulation and a high risk of morbid arterial and venous thrombotic events. Elevated levels of blood neutrophils and neutrophil extracellular traps (NETs) have recently been described in patients with COVID-19. However, their potential role in COVID-19-associated thrombosis remains incompletely understood. In order to elucidate the potential role of hyperactive neutrophils and NET release in COVID19-associated thrombosis, we conducted a case–control study of patients hospitalized with COVID-19 who developed thrombosis, as compared with gender- and age-matched COVID-19 patients without clinical thrombosis. We found that remnants of NETs (cell-free DNA, myeloperoxidase-DNA complexes, and citrullinated histone H3) and neutrophil-derived S100A8/ A9 (calprotectin) in patient sera were associated with higher risk of morbid thrombotic events in spite of prophylactic anticoagulation. These observations underscore the need for urgent investigation into the potential relationship between NETs and unrelenting thrombosis in COVID-19, as well as novel approaches for thrombosis prevention. Keywords Blood coagulation · COVID-19 · Calprotectin · Extracellular traps · Neutrophils · Venous thrombosis
Highlights • Mechanisms contributing to frequent thrombosis in
• Exploring approaches to neutralize neutrophils and NETs
in COVID-19 warrants urgent investigation
COVID-19 remain incompletely understood
Introduction
patients with COVID-19-associated thrombosis
Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) causes the disease known as coronavirus disease 2019 (COVID-19). It most commonly presents with influenza-like illness and viral pneumonia, but in its most severe manifestation progresses to acute respiratory distress syndrome (ARDS) and multi-organ failure [1]. To date the viral
• NETs and neutrophil activation were measured in • Thrombosis in COVID-19 was associated with higher
levels of circulating NETs and calprotectin
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11239-020-02324-z) contains supplementary material, which is available to authorized users. * Jason S. Knight [email protected]
4
Michigan Clinical Research Unit, University of Michigan, Ann Arbor, MI, USA
* Yogendra Kanthi [email protected]
5
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA
1
Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA
6
Division of Geri
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