Interleukin-1 and Stroke: Biomarker, Harbinger of Damage, and Therapeutic Target

被引:99
作者
Denes, Adam [1 ]
Pinteaux, Emmanuel [1 ]
Rothwell, Nancy J. [1 ]
Allan, Stuart M. [1 ]
机构
[1] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England
基金
英国医学研究理事会;
关键词
Interleukin-1; IL-1Ra; ISCHEMIC BRAIN-DAMAGE; RECEPTOR ACCESSORY PROTEIN; TUMOR-NECROSIS-FACTOR; INFLAMMATORY RESPONSE; SYSTEMIC INFECTION; CEREBRAL-ISCHEMIA; GENE POLYMORPHISM; NEURONAL INJURY; NERVOUS-SYSTEM; ANIMAL-MODELS;
D O I
10.1159/000332205
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Inflammation is established as a contributor to cerebrovascular disease. Risk factors for stroke include many conditions associated with chronic or acute inflammation, and inflammatory changes in the brain after cerebrovascular events contribute to outcome in experimental studies, with growing evidence from clinical research. The brain is extremely susceptible to inflammatory challenge, but resident glia, endothelial cells and neurones can all mount a pronounced inflammatory response to infection or injury. Recent discoveries highlight the importance of peripherally-derived immune cells and inflammatory molecules in various central nervous system disorders, including stroke. The inflammatory cytokine, interleukin-1 (IL-1), plays a pivotal role in both local and systemic inflammation, and is a key driver of peripheral and central immune responses to infection or injury. Inhibition of IL-1 has beneficial effects in a variety of experimental paradigms of acute brain injury and is a promising clinical target in stroke. We propose that blockade of IL-1 could be therapeutically useful in several diseases which are risk factors for stroke, and there is already considerable preclinical and clinical evidence that inhibition of IL-1 by IL-1 receptor antagonist may be valuable in the management of acute stroke. Copyright (C) 2011 S. Karger AG, Basel
引用
收藏
页码:517 / 527
页数:11
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