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Extracellular DNA traps promote thrombosis

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Extracellular DNA traps promote thrombosis. / Fuchs, Tobias A; Brill, Alexander; Duerschmied, Daniel; Schatzberg, Daphne; Monestier, Marc; Myers, Daniel D; Wrobleski, Shirley K; Wakefield, Thomas W; Hartwig, John H; Wagner, Denisa D.

In: P NATL ACAD SCI USA, Vol. 107, No. 36, 07.09.2010, p. 15880-5.

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

Harvard

Fuchs, TA, Brill, A, Duerschmied, D, Schatzberg, D, Monestier, M, Myers, DD, Wrobleski, SK, Wakefield, TW, Hartwig, JH & Wagner, DD 2010, 'Extracellular DNA traps promote thrombosis', P NATL ACAD SCI USA, vol. 107, no. 36, pp. 15880-5. https://doi.org/10.1073/pnas.1005743107

APA

Fuchs, T. A., Brill, A., Duerschmied, D., Schatzberg, D., Monestier, M., Myers, D. D., Wrobleski, S. K., Wakefield, T. W., Hartwig, J. H., & Wagner, D. D. (2010). Extracellular DNA traps promote thrombosis. P NATL ACAD SCI USA, 107(36), 15880-5. https://doi.org/10.1073/pnas.1005743107

Vancouver

Fuchs TA, Brill A, Duerschmied D, Schatzberg D, Monestier M, Myers DD et al. Extracellular DNA traps promote thrombosis. P NATL ACAD SCI USA. 2010 Sep 7;107(36):15880-5. https://doi.org/10.1073/pnas.1005743107

Bibtex

@article{843d98b631cc4b039e2009d0c0d47bd8,
title = "Extracellular DNA traps promote thrombosis",
abstract = "Neutrophil extracellular traps (NETs) are part of the innate immune response to infections. NETs are a meshwork of DNA fibers comprising histones and antimicrobial proteins. Microbes are immobilized in NETs and encounter a locally high and lethal concentration of effector proteins. Recent studies show that NETs are formed inside the vasculature in infections and noninfectious diseases. Here we report that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation. NETs perfused with blood caused platelet adhesion, activation, and aggregation. DNase or the anticoagulant heparin dismantled the NET scaffold and prevented thrombus formation. Stimulation of platelets with purified histones was sufficient for aggregation. NETs recruited red blood cells, promoted fibrin deposition, and induced a red thrombus, such as that found in veins. Markers of extracellular DNA traps were detected in a thrombus and plasma of baboons subjected to deep vein thrombosis, an example of inflammation-enhanced thrombosis. Our observations indicate that NETs are a previously unrecognized link between inflammation and thrombosis and may further explain the epidemiological association of infection with thrombosis.",
keywords = "Animals, DNA, Humans, Thrombosis",
author = "Fuchs, {Tobias A} and Alexander Brill and Daniel Duerschmied and Daphne Schatzberg and Marc Monestier and Myers, {Daniel D} and Wrobleski, {Shirley K} and Wakefield, {Thomas W} and Hartwig, {John H} and Wagner, {Denisa D}",
year = "2010",
month = sep,
day = "7",
doi = "10.1073/pnas.1005743107",
language = "English",
volume = "107",
pages = "15880--5",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "36",

}

RIS

TY - JOUR

T1 - Extracellular DNA traps promote thrombosis

AU - Fuchs, Tobias A

AU - Brill, Alexander

AU - Duerschmied, Daniel

AU - Schatzberg, Daphne

AU - Monestier, Marc

AU - Myers, Daniel D

AU - Wrobleski, Shirley K

AU - Wakefield, Thomas W

AU - Hartwig, John H

AU - Wagner, Denisa D

PY - 2010/9/7

Y1 - 2010/9/7

N2 - Neutrophil extracellular traps (NETs) are part of the innate immune response to infections. NETs are a meshwork of DNA fibers comprising histones and antimicrobial proteins. Microbes are immobilized in NETs and encounter a locally high and lethal concentration of effector proteins. Recent studies show that NETs are formed inside the vasculature in infections and noninfectious diseases. Here we report that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation. NETs perfused with blood caused platelet adhesion, activation, and aggregation. DNase or the anticoagulant heparin dismantled the NET scaffold and prevented thrombus formation. Stimulation of platelets with purified histones was sufficient for aggregation. NETs recruited red blood cells, promoted fibrin deposition, and induced a red thrombus, such as that found in veins. Markers of extracellular DNA traps were detected in a thrombus and plasma of baboons subjected to deep vein thrombosis, an example of inflammation-enhanced thrombosis. Our observations indicate that NETs are a previously unrecognized link between inflammation and thrombosis and may further explain the epidemiological association of infection with thrombosis.

AB - Neutrophil extracellular traps (NETs) are part of the innate immune response to infections. NETs are a meshwork of DNA fibers comprising histones and antimicrobial proteins. Microbes are immobilized in NETs and encounter a locally high and lethal concentration of effector proteins. Recent studies show that NETs are formed inside the vasculature in infections and noninfectious diseases. Here we report that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation. NETs perfused with blood caused platelet adhesion, activation, and aggregation. DNase or the anticoagulant heparin dismantled the NET scaffold and prevented thrombus formation. Stimulation of platelets with purified histones was sufficient for aggregation. NETs recruited red blood cells, promoted fibrin deposition, and induced a red thrombus, such as that found in veins. Markers of extracellular DNA traps were detected in a thrombus and plasma of baboons subjected to deep vein thrombosis, an example of inflammation-enhanced thrombosis. Our observations indicate that NETs are a previously unrecognized link between inflammation and thrombosis and may further explain the epidemiological association of infection with thrombosis.

KW - Animals

KW - DNA

KW - Humans

KW - Thrombosis

U2 - 10.1073/pnas.1005743107

DO - 10.1073/pnas.1005743107

M3 - SCORING: Journal article

C2 - 20798043

VL - 107

SP - 15880

EP - 15885

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 36

ER -