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Host DNases prevent vascular occlusion by neutrophil extracellular traps

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Host DNases prevent vascular occlusion by neutrophil extracellular traps. / Jiménez-Alcázar, Miguel; Rangaswamy, Chandini; Panda, Rachita; Bitterling, Josephine; Simsek, Yashin J; Long, Andy T; Bilyy, Rostyslav; Krenn, Veit; Renné, Christoph; Renné, Thomas; Kluge, Stefan; Panzer, Ulf; Mizuta, Ryushin; Mannherz, Hans Georg; Kitamura, Daisuke; Herrmann, Martin; Napirei, Markus; Fuchs, Tobias A.

In: SCIENCE, Vol. 358, No. 6367, 01.12.2017, p. 1202-1206.

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

Harvard

Jiménez-Alcázar, M, Rangaswamy, C, Panda, R, Bitterling, J, Simsek, YJ, Long, AT, Bilyy, R, Krenn, V, Renné, C, Renné, T, Kluge, S, Panzer, U, Mizuta, R, Mannherz, HG, Kitamura, D, Herrmann, M, Napirei, M & Fuchs, TA 2017, 'Host DNases prevent vascular occlusion by neutrophil extracellular traps', SCIENCE, vol. 358, no. 6367, pp. 1202-1206. https://doi.org/10.1126/science.aam8897

APA

Jiménez-Alcázar, M., Rangaswamy, C., Panda, R., Bitterling, J., Simsek, Y. J., Long, A. T., Bilyy, R., Krenn, V., Renné, C., Renné, T., Kluge, S., Panzer, U., Mizuta, R., Mannherz, H. G., Kitamura, D., Herrmann, M., Napirei, M., & Fuchs, T. A. (2017). Host DNases prevent vascular occlusion by neutrophil extracellular traps. SCIENCE, 358(6367), 1202-1206. https://doi.org/10.1126/science.aam8897

Vancouver

Jiménez-Alcázar M, Rangaswamy C, Panda R, Bitterling J, Simsek YJ, Long AT et al. Host DNases prevent vascular occlusion by neutrophil extracellular traps. SCIENCE. 2017 Dec 1;358(6367):1202-1206. https://doi.org/10.1126/science.aam8897

Bibtex

@article{5f3ceb8bbca5497aa9886524794d3d97,
title = "Host DNases prevent vascular occlusion by neutrophil extracellular traps",
abstract = "Platelet and fibrin clots occlude blood vessels in hemostasis and thrombosis. Here we report a noncanonical mechanism for vascular occlusion based on neutrophil extracellular traps (NETs), DNA fibers released by neutrophils during inflammation. We investigated which host factors control NETs in vivo and found that two deoxyribonucleases (DNases), DNase1 and DNase1-like 3, degraded NETs in circulation during sterile neutrophilia and septicemia. In the absence of both DNases, intravascular NETs formed clots that obstructed blood vessels and caused organ damage. Vascular occlusions in patients with severe bacterial infections were associated with a defect to degrade NETs ex vivo and the formation of intravascular NET clots. DNase1 and DNase1-like 3 are independently expressed and thus provide dual host protection against deleterious effects of intravascular NETs.",
keywords = "Journal Article, Research Support, Non-U.S. Gov't",
author = "Miguel Jim{\'e}nez-Alc{\'a}zar and Chandini Rangaswamy and Rachita Panda and Josephine Bitterling and Simsek, {Yashin J} and Long, {Andy T} and Rostyslav Bilyy and Veit Krenn and Christoph Renn{\'e} and Thomas Renn{\'e} and Stefan Kluge and Ulf Panzer and Ryushin Mizuta and Mannherz, {Hans Georg} and Daisuke Kitamura and Martin Herrmann and Markus Napirei and Fuchs, {Tobias A}",
note = "Copyright {\textcopyright} 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.",
year = "2017",
month = dec,
day = "1",
doi = "10.1126/science.aam8897",
language = "English",
volume = "358",
pages = "1202--1206",
journal = "SCIENCE",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "6367",

}

RIS

TY - JOUR

T1 - Host DNases prevent vascular occlusion by neutrophil extracellular traps

AU - Jiménez-Alcázar, Miguel

AU - Rangaswamy, Chandini

AU - Panda, Rachita

AU - Bitterling, Josephine

AU - Simsek, Yashin J

AU - Long, Andy T

AU - Bilyy, Rostyslav

AU - Krenn, Veit

AU - Renné, Christoph

AU - Renné, Thomas

AU - Kluge, Stefan

AU - Panzer, Ulf

AU - Mizuta, Ryushin

AU - Mannherz, Hans Georg

AU - Kitamura, Daisuke

AU - Herrmann, Martin

AU - Napirei, Markus

AU - Fuchs, Tobias A

N1 - Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Platelet and fibrin clots occlude blood vessels in hemostasis and thrombosis. Here we report a noncanonical mechanism for vascular occlusion based on neutrophil extracellular traps (NETs), DNA fibers released by neutrophils during inflammation. We investigated which host factors control NETs in vivo and found that two deoxyribonucleases (DNases), DNase1 and DNase1-like 3, degraded NETs in circulation during sterile neutrophilia and septicemia. In the absence of both DNases, intravascular NETs formed clots that obstructed blood vessels and caused organ damage. Vascular occlusions in patients with severe bacterial infections were associated with a defect to degrade NETs ex vivo and the formation of intravascular NET clots. DNase1 and DNase1-like 3 are independently expressed and thus provide dual host protection against deleterious effects of intravascular NETs.

AB - Platelet and fibrin clots occlude blood vessels in hemostasis and thrombosis. Here we report a noncanonical mechanism for vascular occlusion based on neutrophil extracellular traps (NETs), DNA fibers released by neutrophils during inflammation. We investigated which host factors control NETs in vivo and found that two deoxyribonucleases (DNases), DNase1 and DNase1-like 3, degraded NETs in circulation during sterile neutrophilia and septicemia. In the absence of both DNases, intravascular NETs formed clots that obstructed blood vessels and caused organ damage. Vascular occlusions in patients with severe bacterial infections were associated with a defect to degrade NETs ex vivo and the formation of intravascular NET clots. DNase1 and DNase1-like 3 are independently expressed and thus provide dual host protection against deleterious effects of intravascular NETs.

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1126/science.aam8897

DO - 10.1126/science.aam8897

M3 - SCORING: Journal article

C2 - 29191910

VL - 358

SP - 1202

EP - 1206

JO - SCIENCE

JF - SCIENCE

SN - 0036-8075

IS - 6367

ER -