Multiple mechanisms that prevent excessive brain inflammation

被引:31
作者
Yang, Myung-Soon
Min, Kyoung-Jin
Joe, Eunhye
机构
[1] Ajou Univ, Sch Med, Dept Pharmacol, Suwon 441749, Kyunggi Do, South Korea
[2] Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 441749, Kyunggi Do, South Korea
[3] Ajou Univ, Sch Med, Grad Program Neurosci, Suwon 441749, Kyunggi Do, South Korea
关键词
microglial death; antioxidant enzyme; inflammation; suppressor of cytokine signaling; astrocytes;
D O I
10.1002/jnr.21254
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Inflammation of the injured brain has a double-edged effect. Inflammation protects the brain from infection, but it aggravates injury. Furthermore, brain inflammation is considered a risk factor for neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases. Emerging evidence supports the activation of negative regulatory mechanisms during this process to prevent prolonged and extensive inflammation. The inflammatory stimulators themselves or products of inflammatory cells may induce the expression of negative feedback regulators, such as suppressor of cytokine signaling (SOCS)-family proteins, antioxidant enzymes, and anti-inflammatory cytokines. Furthermore, death of activated microglia (major inflammatory cells in the brain) may regulate brain inflammation. Astrocytes, the most abundant cells in the brain, may also act in preventing microglial overactivation. Therefore, we propose that the extent and duration of brain inflammation is tightly regulated through the cooperation of multiple mechanisms to maximize antipathogenic effects and minimize tissue damage. (C) 2007 Wiley-Liss, Inc.
引用
收藏
页码:2298 / 2305
页数:8
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