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Linking infection and inflammation in acute ischemic stroke

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Linking infection and inflammation in acute ischemic stroke. / Worthmann, H; Tryc, A B; Deb-Chatterji, Milani; Goldbecker, A; Ma, Y T; Tountopoulou, A; Lichtinghagen, R; Weissenborn, K.

in: ANN NY ACAD SCI, Jahrgang 1207, 10.2010, S. 116-22.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Worthmann, H, Tryc, AB, Deb-Chatterji, M, Goldbecker, A, Ma, YT, Tountopoulou, A, Lichtinghagen, R & Weissenborn, K 2010, 'Linking infection and inflammation in acute ischemic stroke', ANN NY ACAD SCI, Jg. 1207, S. 116-22. https://doi.org/10.1111/j.1749-6632.2010.05738.x

APA

Worthmann, H., Tryc, A. B., Deb-Chatterji, M., Goldbecker, A., Ma, Y. T., Tountopoulou, A., Lichtinghagen, R., & Weissenborn, K. (2010). Linking infection and inflammation in acute ischemic stroke. ANN NY ACAD SCI, 1207, 116-22. https://doi.org/10.1111/j.1749-6632.2010.05738.x

Vancouver

Worthmann H, Tryc AB, Deb-Chatterji M, Goldbecker A, Ma YT, Tountopoulou A et al. Linking infection and inflammation in acute ischemic stroke. ANN NY ACAD SCI. 2010 Okt;1207:116-22. https://doi.org/10.1111/j.1749-6632.2010.05738.x

Bibtex

@article{6d622b4211da49379cc4576e07e022cb,
title = "Linking infection and inflammation in acute ischemic stroke",
abstract = "Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.",
keywords = "Brain Ischemia, Humans, Infection, Infection Control, Inflammation, Inflammation Mediators, Neuroimmunomodulation, Prognosis, Stroke, Journal Article, Review",
author = "H Worthmann and Tryc, {A B} and Milani Deb-Chatterji and A Goldbecker and Ma, {Y T} and A Tountopoulou and R Lichtinghagen and K Weissenborn",
note = "{\textcopyright} 2010 New York Academy of Sciences.",
year = "2010",
month = oct,
doi = "10.1111/j.1749-6632.2010.05738.x",
language = "English",
volume = "1207",
pages = "116--22",
journal = "ANN NY ACAD SCI",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

RIS

TY - JOUR

T1 - Linking infection and inflammation in acute ischemic stroke

AU - Worthmann, H

AU - Tryc, A B

AU - Deb-Chatterji, Milani

AU - Goldbecker, A

AU - Ma, Y T

AU - Tountopoulou, A

AU - Lichtinghagen, R

AU - Weissenborn, K

N1 - © 2010 New York Academy of Sciences.

PY - 2010/10

Y1 - 2010/10

N2 - Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.

AB - Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.

KW - Brain Ischemia

KW - Humans

KW - Infection

KW - Infection Control

KW - Inflammation

KW - Inflammation Mediators

KW - Neuroimmunomodulation

KW - Prognosis

KW - Stroke

KW - Journal Article

KW - Review

U2 - 10.1111/j.1749-6632.2010.05738.x

DO - 10.1111/j.1749-6632.2010.05738.x

M3 - SCORING: Journal article

C2 - 20955434

VL - 1207

SP - 116

EP - 122

JO - ANN NY ACAD SCI

JF - ANN NY ACAD SCI

SN - 0077-8923

ER -