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Novel cell death program leads to neutrophil extracellular traps

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Novel cell death program leads to neutrophil extracellular traps. / Fuchs, Tobias A; Abed, Ulrike; Goosmann, Christian; Hurwitz, Robert; Schulze, Ilka; Wahn, Volker; Weinrauch, Yvette; Brinkmann, Volker; Zychlinsky, Arturo.

In: J CELL BIOL, Vol. 176, No. 2, 15.01.2007, p. 231-41.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Fuchs, TA, Abed, U, Goosmann, C, Hurwitz, R, Schulze, I, Wahn, V, Weinrauch, Y, Brinkmann, V & Zychlinsky, A 2007, 'Novel cell death program leads to neutrophil extracellular traps', J CELL BIOL, vol. 176, no. 2, pp. 231-41. https://doi.org/10.1083/jcb.200606027

APA

Fuchs, T. A., Abed, U., Goosmann, C., Hurwitz, R., Schulze, I., Wahn, V., Weinrauch, Y., Brinkmann, V., & Zychlinsky, A. (2007). Novel cell death program leads to neutrophil extracellular traps. J CELL BIOL, 176(2), 231-41. https://doi.org/10.1083/jcb.200606027

Vancouver

Fuchs TA, Abed U, Goosmann C, Hurwitz R, Schulze I, Wahn V et al. Novel cell death program leads to neutrophil extracellular traps. J CELL BIOL. 2007 Jan 15;176(2):231-41. https://doi.org/10.1083/jcb.200606027

Bibtex

@article{1e9ba09a784e450c9d57fa5f8da35bec,
title = "Novel cell death program leads to neutrophil extracellular traps",
abstract = "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.",
keywords = "Antibodies, Antigens, CD95, Apoptosis, Catalase, Cell Death, Cell Survival, Chromatin, Cytoplasmic Granules, Enzyme Inhibitors, Granulomatous Disease, Chronic, Humans, Hydrogen Peroxide, Immunity, Innate, Leukocyte Elastase, Microscopy, Electron, NADPH Oxidase, Neutrophil Activation, Neutrophils, Nuclear Envelope, Onium Compounds, Phagocytosis, Reactive Oxygen Species, Staphylococcus aureus, Tetradecanoylphorbol Acetate, Vacuoles",
author = "Fuchs, {Tobias A} and Ulrike Abed and Christian Goosmann and Robert Hurwitz and Ilka Schulze and Volker Wahn and Yvette Weinrauch and Volker Brinkmann and Arturo Zychlinsky",
year = "2007",
month = jan,
day = "15",
doi = "10.1083/jcb.200606027",
language = "English",
volume = "176",
pages = "231--41",
journal = "J CELL BIOL",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Novel cell death program leads to neutrophil extracellular traps

AU - Fuchs, Tobias A

AU - Abed, Ulrike

AU - Goosmann, Christian

AU - Hurwitz, Robert

AU - Schulze, Ilka

AU - Wahn, Volker

AU - Weinrauch, Yvette

AU - Brinkmann, Volker

AU - Zychlinsky, Arturo

PY - 2007/1/15

Y1 - 2007/1/15

N2 - 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.

AB - 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.

KW - Antibodies

KW - Antigens, CD95

KW - Apoptosis

KW - Catalase

KW - Cell Death

KW - Cell Survival

KW - Chromatin

KW - Cytoplasmic Granules

KW - Enzyme Inhibitors

KW - Granulomatous Disease, Chronic

KW - Humans

KW - Hydrogen Peroxide

KW - Immunity, Innate

KW - Leukocyte Elastase

KW - Microscopy, Electron

KW - NADPH Oxidase

KW - Neutrophil Activation

KW - Neutrophils

KW - Nuclear Envelope

KW - Onium Compounds

KW - Phagocytosis

KW - Reactive Oxygen Species

KW - Staphylococcus aureus

KW - Tetradecanoylphorbol Acetate

KW - Vacuoles

U2 - 10.1083/jcb.200606027

DO - 10.1083/jcb.200606027

M3 - SCORING: Journal article

C2 - 17210947

VL - 176

SP - 231

EP - 241

JO - J CELL BIOL

JF - J CELL BIOL

SN - 0021-9525

IS - 2

ER -