Neutrophil Extracellular Traps Affecting Cardiovascular Health in Infectious and Inflammatory Diseases.
Manovriti Thakur,Bryce R. Evans,Marc Schindewolf,Iris Baumgartner,Yvonne Döring,Yvonne Döring +5 more
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TLDR
Neutrophil extracellular traps (NETs) are web-like structures of decondensed extracellular chromatin fibers and neutrophil granule proteins released by neutrophils.Abstract:
Neutrophil extracellular traps (NETs) are web-like structures of decondensed extracellular chromatin fibers and neutrophil granule proteins released by neutrophils. NETs participate in host immune defense by entrapping pathogens. They are pro-inflammatory in function, and they act as an initiator of vascular coagulopathies by providing a platform for the attachment of various coagulatory proteins. NETs are diverse in their ability to alter physiological and pathological processes including infection and inflammation. In this review, we will summarize recent findings on the role of NETs in bacterial/viral infections associated with vascular inflammation, thrombosis, atherosclerosis and autoimmune disorders. Understanding the complex role of NETs in bridging infection and chronic inflammation as well as discussing important questions related to their contribution to pathologies outlined above may pave the way for future research on therapeutic targeting of NETs applicable to specific infections and inflammatory disorders.read more
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References
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Neutrophil extracellular traps induced by IL-8 aggravate atherosclerosis via activation NF-κB signaling in macrophages.
Zhujun An,Jiawen Li,Jiangbo Yu,Xiaoli Wang,Hailai Gao,Wei Zhang,Zeren Wei,Jianchun Zhang,Yinli Zhang,Jiyi Zhao,Xiao Liang +10 more
TL;DR: The data reveal a neutrophil-macrophage interaction in AS progression, and indicate that NETs represent as a novel therapeutic target in treatment of AS and other cardiovascular diseases (CVD).
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α-enolase of Streptococcus pneumoniae induces formation of neutrophil extracellular traps
TL;DR: The results indicate that α-enolase from S. pneumoniae increases neutrophil migrating activity and induces cell death of human neutrophils by releasing neutrophIL extracellular traps.
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Neutrophil extracellular trap-microparticle complexes enhance thrombin generation via the intrinsic pathway of coagulation in mice.
Yongzhi Wang,Lingtao Luo,Lingtao Luo,Oscar Ö. Braun,Johannes Westman,Raed Madhi,Heiko Herwald,Matthias Mörgelin,Henrik Thorlacius +8 more
TL;DR: It is concluded that NET-MP complexes induce thrombin generation via the intrinsic pathway of coagulation and that neutrophil-derived MPs play a key role in NET-dependent coagulations.
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Neutrophil Extracellular Traps Promote Inflammatory Responses in Psoriasis via Activating Epidermal TLR4/IL-36R Crosstalk
Shuai Shao,Hui Fang,Erle Dang,Ke Xue,Jieyu Zhang,Bing Li,Hongjiang Qiao,Tianyu Cao,Yuchen Zhuang,Shengxian Shen,T. Zhang,Pei Qiao,Caixia Li,Johann E. Gudjonsson,Gang Wang +14 more
TL;DR: It is demonstrated that NETs drive inflammatory responses in skin through activation of epidermal TLR4/IL-36R crosstalk, and the mechanisms for the proinflammatory activity of NETs in skin are outlined to identify NETs/TLR4 as novel therapeutic targets in psoriasis.
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Neutrophil extracellular traps promote macrophage inflammation and impair atherosclerosis resolution in diabetic mice.
Tatjana Josefs,Tessa J. Barrett,Emily J. Brown,Alexandra Quezada,Xiaoyun Wu,Maud Voisin,Jaume Amengual,Edward A. Fisher +7 more
TL;DR: In diabetic mice deoxyribonuclease 1 (DNase1) treatment reduced plaque NETs content and macrophage inflammation, promoting atherosclerosis resolution after lipid-lowering, and these data suggest that NETs contribute to the increased cardiovascular disease risk in this population and are a potential therapeutic target.