scholarly journals ETosis: A Microbicidal Mechanism beyond Cell Death

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
Keyword(s):  
Cell Death ◽  
Mast Cells ◽  
Cell Types ◽  
Neutrophil Extracellular Traps ◽  
Protozoan Parasites ◽  
Extracellular Milieu ◽  
Extracellular Traps ◽  
Cytoplasmic Proteins

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.

scholarly journals Neutrophil extracellular traps: Is immunity the second function of chromatin?

2012 ◽  
Vol 198 (5) ◽  
pp. 773-783 ◽  
Author(s):  
Volker Brinkmann ◽  
Arturo Zychlinsky
Keyword(s):  
Cell Death ◽  
Blood Cells ◽  
White Blood Cells ◽  
Neutrophil Extracellular Traps ◽  
Unique Form ◽  
Danger Signals ◽  
Extracellular Traps ◽  
Cytoplasmic Proteins ◽  
Microbial Infections

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.

scholarly journals Neutrophil extracellular traps mediate transfer of cytoplasmic neutrophil antigens to myeloid dendritic cells toward ANCA induction and associated autoimmunity

Blood ◽  
2012 ◽  
Vol 120 (15) ◽  
pp. 3007-3018 ◽  
Author(s):  
Sabina Sangaletti ◽  
Claudio Tripodo ◽  
Claudia Chiodoni ◽  
Carla Guarnotta ◽  
Barbara Cappetti ◽  
...  
Keyword(s):  
Cell Death ◽  
Dendritic Cells ◽  
Structural Integrity ◽  
Neutrophil Extracellular Traps ◽  
Antineutrophil Cytoplasmic Antibodies ◽  
Small Vessel Vasculitis ◽  
Myeloid Dendritic Cells ◽  
Extracellular Traps ◽  
Cytoplasmic Proteins ◽  
Human Pathology

Abstract Antineutrophil cytoplasmic antibodies (ANCAs) target proteins normally retained within neutrophils, indicating that cell death is involved in the autoimmunity process. Still, ANCA pathogenesis remains obscure. ANCAs activate neutrophils inducing their respiratory burst and a peculiar form of cell death, named NETosis, characterized by formation of neutrophil extracellular traps (NETs), decondensed chromatin threads decorated with cytoplasmic proteins endorsed with antimicrobial activity. NETs have been consistently detected in ANCA-associated small-vessel vasculitis, and this association prompted us to test whether the peculiar structure of NET favors neutrophil proteins uploading into myeloid dendritic cells and the induction of ANCAs and associated autoimmunity. Here we show that myeloid DCs uploaded with and activated by NET components induce ANCA and autoimmunity when injected into naive mice. DC uploading and autoimmunity induction are prevented by NET treatment with DNAse, indicating that NET structural integrity is needed to maintain the antigenicity of cytoplasmic proteins. We found NET intermingling with myeloid dendritic cells also positive for neutrophil myeloperoxidase in myeloperoxidase-ANCA-associated microscopic poliangiitis providing a potential correlative picture in human pathology. These data provide the first demonstration that NET structures are highly immunogenic such to trigger adaptive immune response relevant for autoimmunity.

scholarly journals Staphylococcus aureus Degrades Neutrophil Extracellular Traps to Promote Immune Cell Death

Science ◽  
2013 ◽  
Vol 342 (6160) ◽  
pp. 863-866 ◽  
Author(s):  
V. Thammavongsa ◽  
D. M. Missiakas ◽  
O. Schneewind
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Immune Cell ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

NETosis: how vital is it?

Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2784-2794 ◽  
Author(s):  
Bryan G. Yipp ◽  
Paul Kubes
Keyword(s):  
Innate Immunity ◽  
Cell Death ◽  
Critical Role ◽  
Neutrophil Extracellular Traps ◽  
Live Cell ◽  
Extracellular Traps ◽  
Cell Death Pathway ◽  
A Cell ◽  
Net Release

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.

scholarly journals Netome: The Molecular Characterization of Neutrophil Extracellular Traps (NETs)

2020 ◽  
Author(s):  
David Scieszka ◽  
Yi-Han Lin ◽  
Weizhong Li ◽  
Saibyasachi Choudhury ◽  
Yanbao Yu ◽  
...  
Keyword(s):  
Antimicrobial Agents ◽  
Genomic Sequence ◽  
White Blood Cells ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Dna ◽  
Sterile Inflammation ◽  
Extracellular Milieu ◽  
Extracellular Traps ◽  
Genomics And Proteomics

AbstractNeutrophils are the most abundant type of white blood cells in humans with biological roles relevant to inflammation and fighting infections. The release of neutrophil extracellular DNA aims to control invasion by bacteria, viruses, fungi, and tissue damage. Neutrophil Extracellular Traps (NETs) act as antimicrobial agents triggering immune signaling through the release of the nuclear content into the extracellular space. Although intense investigations have elucidated the pathways preceding NET formation, the exact molecular composition of released NETs has not been mapped. We aimed to decode the sequences of DNA and proteins from NETs. With emerging needs to understand neutrophil functions precisely, we open the field of NETOMIC studies through isolation of NETs in combination with omics approaches including shotgun genomics and proteomics. Our in vitro NET isolation methodology allowed for unprecedented replicability with induction in a sterile inflammation model system. Enrichment of mitochondrial DNA and telomere sequences are significantly expressed in NET genomes. This study revealed that the genomic sequence released in the extracellular milieu is not stochastically serving as a scaffold for a repertoire of proteins involved in neutrophil protective functions. Collectively, we established the gene and protein signatures exclusive to the extracellular NETs in comparison to undifferentiated and differentiated neutrophil states, further guiding future detection of specific regions needed for diagnostics and targeted therapies of NET related conditions.

scholarly journals Novel cell death program leads to neutrophil extracellular traps

2007 ◽  
Vol 204 (1) ◽  
pp. i2-i2 ◽  
Author(s):  
Tobias A. Fuchs ◽  
Ulrike Abed ◽  
Christian Goosmann ◽  
Robert Hurwitz ◽  
Ilka Schulze ◽  
...  
Keyword(s):  
Cell Death ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Cell Death Program

scholarly journals Novel cell death program leads to neutrophil extracellular traps

2007 ◽  
Vol 176 (2) ◽  
pp. 231-241 ◽  
Author(s):  
Tobias A. Fuchs ◽  
Ulrike Abed ◽  
Christian Goosmann ◽  
Robert Hurwitz ◽  
Ilka Schulze ◽  
...  
Keyword(s):  
Cell Death ◽  
Nadph Oxidase ◽  
Neutrophil Extracellular Traps ◽  
Death Process ◽  
Extracellular Traps ◽  
Cell Death Pathway ◽  
Antimicrobial Function ◽  
Cell Death Program ◽  
Cell Death Process ◽  
Extracellular Structures

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.

scholarly journals The regulatory mechanism of neutrophil extracellular traps in cancer biological behavior

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hui Wang ◽  
Yiyin Zhang ◽  
Qianling Wang ◽  
Xiaoli Wei ◽  
Hua Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Defense ◽  
Regulatory Mechanism ◽  
Neutrophil Extracellular Traps ◽  
Biological Behavior ◽  
Molecular Pathways ◽  
The Past ◽  
Extracellular Traps ◽  
Promote Tumor Growth ◽  
Cancer Associated Thrombosis

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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