Inflammatory Mechanisms after Ischemia and Stroke

Inflammation has been implicated as a secondary injury mechanism following ischemia and stroke. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate the importance of inflammation. The vasculature endothelium promotes inflammation t...

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Bibliographic Details
Published in:Journal of neuropathology and experimental neurology 2003-02, Vol.62 (2), p.127-136
Main Authors: DANTON, GARY H, DIETRICH, W DALTON
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain Ischemia - immunology
Brain Ischemia - metabolism
Brain Ischemia - physiopathology
Cell Adhesion Molecules - immunology
Cell Adhesion Molecules - metabolism
Chemotaxis, Leukocyte - physiology
Disease Models, Animal
Encephalitis - immunology
Encephalitis - metabolism
Encephalitis - physiopathology
Humans
Medical sciences
Microcirculation - immunology
Microcirculation - metabolism
Microcirculation - physiopathology
Neurology
Stroke - immunology
Stroke - metabolism
Stroke - physiopathology
Vascular diseases and vascular malformations of the nervous system
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Summary:Inflammation has been implicated as a secondary injury mechanism following ischemia and stroke. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate the importance of inflammation. The vasculature endothelium promotes inflammation through the upregulation of adhesion molecules such as ICAM, E-selectin, and P-selectin that bind to circulating leukocytes and facilitate their migration into the CNS. Once in the CNS, the production of cytotoxic molecules may facilitate cell death. The macrophage and microglial response to injury may either be beneficial by scavenging necrotic debris or detrimental by facilitating cell death in neurons that would otherwise recover. While many studies have tested these hypotheses, the importance of inflammation in these models is inconclusive. This review summarizes data regarding the role of the vasculature, leukocytes, blood-brain barrier, macrophages, and microglia after experimental and clinical stroke.
ISSN:0022-3069
1554-6578
DOI:10.1093/jnen/62.2.127