IL-1β Enhances the Antibacterial Activity of Astrocytes by Activation of NF-κB

被引:13
|
作者
Xia, Yulei [1 ]
Zhai, Qiwei [1 ]
机构
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab,Grad Sch, Shanghai 200031, Peoples R China
基金
中国国家自然科学基金;
关键词
glia; translocation; I kappa B alpha; Escherichia coli; INNATE IMMUNITY; EXPRESSION; MICROGLIA; RECEPTOR; BRAIN; LIPOPOLYSACCHARIDE; TRANSCRIPTION; MECHANISM; RESPONSES; SIGNALS;
D O I
10.1002/glia.20921
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Astrocytes have important immune functions in CNS, and astrocytes stimulated by interferon-gamma were showed to have direct antimicrobial function. However whether astrocytes without the stimulation of cytokines have antibacterial function, and how this function is regulated are still largely unknown. In this study, we found that primary cultured astrocytes inhibited the growth of both gram-negative and gram-positive bacteria. Further more, we showed that interleukin-1 beta (IL-1 beta) enhanced the antibacterial effect in a dose-dependent manner, and the antibacterial effect of astrocytes from IL-1 beta receptor-deficient mice failed to be enhanced by IL-1 beta. IL-1 beta stimulated I kappa B alpha degradation, NF-kappa B nuclear translocation, and transactivation in astrocytes. NF-kappa B inhibitors blocked NF-kappa B activation and the enhanced antibacterial effect induced by IL-1 beta. In addition, overexpression of dominant negative I kappa B alpha in astrocytes inhibited I kappa B alpha degradation and NF-kappa B transactivation, and also inhibited the enhanced antibacterial effect induced by IL-1 beta. All these data demonstrated that IL-1 beta enhanced the antibacterial activity of astrocytes by activation of NF-kappa B. (C) 2009 WilLy-Liss, Inc.
引用
收藏
页码:244 / 252
页数:9
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