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, Vol. 1207, 10.2010, p. 116-22.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -