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Journal ArticleDOI

The pathway of neutrophil extracellular traps towards atherosclerosis and thrombosis

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TLDR
It has been demonstrated that NETs are present in atherosclerotic lesions of both humans and animal models and are implicated in various mechanisms leading to atherogenesis, and NETs promote the accumulation of prothrombotic molecules, thus significantly contributing to thrombus formation.
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This article is published in Atherosclerosis.The article was published on 2019-09-01. It has received 89 citations till now. The article focuses on the topics: Neutrophil extracellular traps.

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Neutrophil Extracellular Traps Participate in Cardiovascular Diseases: Recent Experimental and Clinical Insights.

TL;DR: This review presents current concepts of neutrophil biology, the triggers to and mechanisms of NET formation, and the contribution ofNETs to atherosclerosis and to thrombosis, and considers the use of markers of NETs in clinical studies.
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NETosis: Molecular Mechanisms, Role in Physiology and Pathology.

TL;DR: Basic mechanisms of NETosis, as well as its role in the pathogenesis of some diseases including COVID-19 are discussed.
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Metformin, Macrophage Dysfunction and Atherosclerosis.

TL;DR: In this article, the authors discussed the future research directions of metformin: single-cell RNA sequencing, neutrophil extracellular traps (NETs), epigenetic modification, and metin-based combination drugs.
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Immune complexes, innate immunity, and NETosis in ChAdOx1 vaccine-induced thrombocytopenia.

Abstract: Aims We recently reported five cases of vaccine-induced immune thrombotic thrombocytopenia (VITT) 7-10 days after receiving the first dose of the ChAdOx1 nCoV-19 adenoviral vector vaccine against corona virus disease 2019 (COVID-19). We aimed to investigate the pathogenic immunological responses operating in these patients. Methods and results We assessed circulating inflammatory markers by immune assays and immune cell phenotyping by flow cytometry analyses and performed immunoprecipitation with anti-platelet factor (PF)4 antibody in plasma samples followed by mass spectrometry from all five patients. A thrombus was retrieved from the sinus sagittal superior of one patient and analysed by immunohistochemistry and flow cytometry. Precipitated immune complexes revealed multiple innate immune pathway triggers for platelet and leucocyte activation. Plasma contained increased levels of innate immune response cytokines and markers of systemic inflammation, extensive degranulation of neutrophils, and tissue and endothelial damage. Blood analyses showed activation of neutrophils and increased levels of circulating H3Cit, dsDNA, and myeloperoxidase-DNA complex. The thrombus had extensive infiltration of neutrophils, formation of neutrophil extracellular traps (NETs), and IgG deposits. Conclusions The results show that anti-PF4/polyanion IgG-mediated thrombus formation in VITT patients is accompanied by a massive innate immune activation and particularly the fulminant activation of neutrophils including NETosis. These results provide novel data on the immune response in this rare adenoviral vector-induced VITT.
References
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Journal ArticleDOI

Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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Novel cell death program leads to neutrophil extracellular traps

TL;DR: This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan.
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Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood

TL;DR: It is proposed that platelet TLR4 is a threshold switch for this new bacterial trapping mechanism in severe sepsis, where NETs have the greatest capacity for bacterial trapping.
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Extracellular DNA traps promote thrombosis

TL;DR: It is reported that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation and may further explain the epidemiological association of infection with thrombosis.
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Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps

TL;DR: Neutrophil elastase escapes azurophilic granules, translocates to the nucleus, and degrades histones to promote chromatin decondensation necessary for NET formation.
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