Platelets and infection

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Platelets and infection. / Deppermann, Carsten; Kubes, Paul.

in: SEMIN IMMUNOL, Jahrgang 28, Nr. 6, 12.2016, S. 536-545.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

Harvard

Deppermann, C & Kubes, P 2016, 'Platelets and infection', SEMIN IMMUNOL, Jg. 28, Nr. 6, S. 536-545. https://doi.org/10.1016/j.smim.2016.10.005

APA

Deppermann, C., & Kubes, P. (2016). Platelets and infection. SEMIN IMMUNOL, 28(6), 536-545. https://doi.org/10.1016/j.smim.2016.10.005

Vancouver

Bibtex

@article{7f5493d5d0584d999c94d7fe0bf804c7,
title = "Platelets and infection",
abstract = "The primary function of platelets is to patrol the vasculature and seal vessel breaches to limit blood loss. However, it is becoming increasingly clear that they also contribute to pathophysiological conditions like thrombosis, atherosclerosis, stroke and infection. Severe sepsis is a devastating disease that claims hundreds of thousands of lives every year in North America and is a major burden to the public health system. Platelet surface receptors like GPIb, αIIbβ3, TLR2 and TLR4 are involved in direct platelet-bacteria interactions. Plasma proteins like fibrinogen and vWF enable indirect interactions. Furthermore, platelet granules contain a plethora of proteins that modulate the immune response as well as microbicidal agents which can directly lyse bacteria. Bacterial toxins are potent platelet activators and can cause intravascular platelet aggregation. Platelets contribute to the antibacterial response of the host involving Kupffer cells, neutrophils and the complement system. In this review we summarize the current knowledge about platelet-bacteria interactions and highlight recent advances in the field.",
keywords = "Animals, Bacterial Toxins/immunology, Blood Platelets/immunology, Cell Communication, Cytoplasmic Granules/metabolism, Host-Pathogen Interactions/immunology, Humans, Infections/etiology, Macrophages/immunology, Neutrophils/immunology, Platelet Activation/immunology, Platelet Membrane Glycoproteins/immunology, Sepsis/etiology, Signal Transduction",
author = "Carsten Deppermann and Paul Kubes",
note = "Crown Copyright {\textcopyright} 2016. Published by Elsevier Ltd. All rights reserved.",
year = "2016",
month = dec,
doi = "10.1016/j.smim.2016.10.005",
language = "English",
volume = "28",
pages = "536--545",
journal = "SEMIN IMMUNOL",
issn = "1044-5323",
publisher = "Academic Press Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Platelets and infection

AU - Deppermann, Carsten

AU - Kubes, Paul

N1 - Crown Copyright © 2016. Published by Elsevier Ltd. All rights reserved.

PY - 2016/12

Y1 - 2016/12

N2 - The primary function of platelets is to patrol the vasculature and seal vessel breaches to limit blood loss. However, it is becoming increasingly clear that they also contribute to pathophysiological conditions like thrombosis, atherosclerosis, stroke and infection. Severe sepsis is a devastating disease that claims hundreds of thousands of lives every year in North America and is a major burden to the public health system. Platelet surface receptors like GPIb, αIIbβ3, TLR2 and TLR4 are involved in direct platelet-bacteria interactions. Plasma proteins like fibrinogen and vWF enable indirect interactions. Furthermore, platelet granules contain a plethora of proteins that modulate the immune response as well as microbicidal agents which can directly lyse bacteria. Bacterial toxins are potent platelet activators and can cause intravascular platelet aggregation. Platelets contribute to the antibacterial response of the host involving Kupffer cells, neutrophils and the complement system. In this review we summarize the current knowledge about platelet-bacteria interactions and highlight recent advances in the field.

AB - The primary function of platelets is to patrol the vasculature and seal vessel breaches to limit blood loss. However, it is becoming increasingly clear that they also contribute to pathophysiological conditions like thrombosis, atherosclerosis, stroke and infection. Severe sepsis is a devastating disease that claims hundreds of thousands of lives every year in North America and is a major burden to the public health system. Platelet surface receptors like GPIb, αIIbβ3, TLR2 and TLR4 are involved in direct platelet-bacteria interactions. Plasma proteins like fibrinogen and vWF enable indirect interactions. Furthermore, platelet granules contain a plethora of proteins that modulate the immune response as well as microbicidal agents which can directly lyse bacteria. Bacterial toxins are potent platelet activators and can cause intravascular platelet aggregation. Platelets contribute to the antibacterial response of the host involving Kupffer cells, neutrophils and the complement system. In this review we summarize the current knowledge about platelet-bacteria interactions and highlight recent advances in the field.

KW - Animals

KW - Bacterial Toxins/immunology

KW - Blood Platelets/immunology

KW - Cell Communication

KW - Cytoplasmic Granules/metabolism

KW - Host-Pathogen Interactions/immunology

KW - Humans

KW - Infections/etiology

KW - Macrophages/immunology

KW - Neutrophils/immunology

KW - Platelet Activation/immunology

KW - Platelet Membrane Glycoproteins/immunology

KW - Sepsis/etiology

KW - Signal Transduction

U2 - 10.1016/j.smim.2016.10.005

DO - 10.1016/j.smim.2016.10.005

M3 - SCORING: Review article

C2 - 27769639

VL - 28

SP - 536

EP - 545

JO - SEMIN IMMUNOL

JF - SEMIN IMMUNOL

SN - 1044-5323

IS - 6

ER -