Inflammatory and Neuroimmunomodulatory Changes in Acute Cerebral Ischemia

被引:78
作者
Brea, David [1 ]
Sobrino, Tomas [1 ]
Ramos-Cabrer, Pedro [1 ]
Castillo, Jose [1 ]
机构
[1] Univ Santiago de Compostela, Hosp Clin Univ Santiago de Compostela, Dept Neurol, Clin Neurosci Res Lab, Santiago De Compostela, Spain
关键词
Inflammation; Immunomodulation; Stroke; Innate immunity; Adaptive immunity; TUMOR-NECROSIS-FACTOR; INTERCELLULAR-ADHESION MOLECULE-1; TOLL-LIKE RECEPTORS; COLONY-STIMULATING FACTOR; NITRIC-OXIDE SYNTHASE; MONOCYTE CHEMOATTRACTANT PROTEIN-1; INTERLEUKIN-1-BETA MESSENGER-RNA; BLOOD-BRAIN-BARRIER; GROWTH-FACTOR-BETA; FACTOR-KAPPA-B;
D O I
10.1159/000200441
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Neuronal death produced by cerebral ischemia activates innate immunity by Toll-like receptors and triggers inflammatory response. This response is necessary to remove cell debris and to start regenerative process. However, inflammatory response could exacerbate cerebral damage and it is involved in secondary brain damage. Therefore, organisms have developed different mechanisms to regulate inflammatory response. An accurate balance between inflammation and anti-inflammation is necessary to assure the removal of cell debris and to avoid secondary cell damage. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral brain damage after cerebral ischemia. In this paper, we review the function of the immune system in cerebral ischemia, particularly inflammation and immunomodulation. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:48 / 64
页数:17
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