Faculty Opinions recommendation of Novel cell death program leads to neutrophil extracellular traps.

Author(s):  
Eric Denkers
2007 ◽  
Vol 176 (2) ◽  
pp. 231-241 ◽  
Author(s):  
Tobias A. Fuchs ◽  
Ulrike Abed ◽  
Christian Goosmann ◽  
Robert Hurwitz ◽  
Ilka Schulze ◽  
...  

Neutrophil extracellular traps (NETs) are extracellular structures composed of chromatin and granule proteins that bind and kill microorganisms. We show that upon stimulation, the nuclei of neutrophils lose their shape, and the eu- and heterochromatin homogenize. Later, the nuclear envelope and the granule membranes disintegrate, allowing the mixing of NET components. Finally, the NETs are released as the cell membrane breaks. This cell death process is distinct from apoptosis and necrosis and depends on the generation of reactive oxygen species (ROS) by NADPH oxidase. Patients with chronic granulomatous disease carry mutations in NADPH oxidase and cannot activate this cell-death pathway or make NETs. This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan.


2007 ◽  
Vol 204 (1) ◽  
pp. i2-i2 ◽  
Author(s):  
Tobias A. Fuchs ◽  
Ulrike Abed ◽  
Christian Goosmann ◽  
Robert Hurwitz ◽  
Ilka Schulze ◽  
...  

Science ◽  
2013 ◽  
Vol 342 (6160) ◽  
pp. 863-866 ◽  
Author(s):  
V. Thammavongsa ◽  
D. M. Missiakas ◽  
O. Schneewind

Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2784-2794 ◽  
Author(s):  
Bryan G. Yipp ◽  
Paul Kubes

Abstract In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innate immunity. We summarize how NETs are formed in response to various stimuli and provide evidence that NETosis is not universally a cell death pathway. Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis. We also evaluate the evidence for NETs in catching and killing pathogens. Finally, we examine how infections are related to the development of autoimmune and vasculitic diseases through unintended but detrimental bystander damage resulting from NET release.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Anderson B. Guimarães-Costa ◽  
Michelle T. C. Nascimento ◽  
Amanda B. Wardini ◽  
Lucia H. Pinto-da-Silva ◽  
Elvira M. Saraiva

Netosis is a recently described type of neutrophil death occurring with the release to the extracellular milieu of a lattice composed of DNA associated with histones and granular and cytoplasmic proteins. These webs, initially named neutrophil extracellular traps (NETs), ensnare and kill microorganisms. Similarly, other cell types, such as eosinophils, mast cells, and macrophages, can also dye by this mechanism; thus, it was renamed as ETosis, meaning death with release of extracellular traps (ETs). Here, we review the mechanism of NETosis/etosis, emphasizing its role in diseases caused by protozoan parasites, fungi, and viruses.


2012 ◽  
Vol 198 (5) ◽  
pp. 773-783 ◽  
Author(s):  
Volker Brinkmann ◽  
Arturo Zychlinsky

Neutrophil extracellular traps (NETs) are made of processed chromatin bound to granular and selected cytoplasmic proteins. NETs are released by white blood cells called neutrophils, maybe as a last resort, to control microbial infections. This release of chromatin is the result of a unique form of cell death, dubbed “NETosis.” Here we review our understanding of how NETs are made, their function in infections and as danger signals, and their emerging importance in autoimmunity and coagulation.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hui Wang ◽  
Yiyin Zhang ◽  
Qianling Wang ◽  
Xiaoli Wei ◽  
Hua Wang ◽  
...  

AbstractAs the predominant host defense against pathogens, neutrophil extracellular traps (NETs) have attracted increasing attention due to their vital roles in infectious inflammation in the past few years. Interestingly, NETs also play important roles in noninfectious conditions, such as rheumatism and cancer. The process of NETs formation can be regulated and the form of cell death accompanied by the formation of NETs is regarded as “NETosis”. A large amount of evidence has confirmed that many stimuli can facilitate the release of NETs from neutrophils. Furthermore, it has been illustrated that NETs promote tumor growth and progression via many molecular pathways. Meanwhile, NETs also can promote metastasis in many kinds of cancers based on multiple studies. In addition, some researchs have found that NETs can promote coagulation and cancer-associated thrombosis. In the present review, it will highlight how NETosis, which is stimulated by various stimuli and signaling pathways, affects cancer biological behaviors via NETs. Given their crucial roles in cancer, NETs will become possible therapeutic targets for inhibiting proliferation, metastasis and thrombosis in cancer patients.


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