Lipopolysaccharide and hypoxia/ischemia induced IL-2 expression by microglia in neonatal brain
Lipopolysaccharide and hypoxia/ischemia induced IL-2 expression by microglia in neonatal brain
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DOI：
10.1097/wnr.0b013e3283036e88
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发表时间：
2008-07-02
期刊：
影响因子：
1.7
通讯作者：
Sebire, Guillaume
中科院分区：
文献类型：
--
作者：
Girard, Sylvie;Larouche, Annie;Sebire, Guillaume
利用脂多糖和缺氧/缺血诱导的围产期脑损伤模型，我们假设白细胞介素-2（IL-2），一种神经毒性细胞因子，在受伤的大脑内增强。我们发现，脂多糖和缺氧/缺血增强脑内IL-2 mRNA和蛋白水平，最大增加后脂多糖和缺氧/缺血。缺乏可检测到的T淋巴细胞，表明神经细胞合成IL-2。脂多糖和缺氧刺激培养的小胶质细胞合成IL-2，并在脂多糖和缺氧刺激后达到高峰。双标记表明，在体内和体外，IL-2免疫反应性与小胶质细胞/巨噬细胞标记物共定位。这些结果揭示了小胶质细胞产生IL-2的能力，也表明IL-2在由围产期脂多糖和缺氧/缺血暴露引发的神经细胞死亡中的意义。
Using a model of perinatal brain lesions induced by lipopolysaccharide and hypoxia/ischemia, we hypothesized that interleukin-2 (IL-2), a neurotoxic cytokine, was enhanced within injured brains. We showed that lipopolysaccharide and hypoxia/ischemia enhanced both intracerebral IL-2 mRNA and protein levels, with a maximum increase upon lipopolysaccharide and hypoxia/ischemia. The lack of detectable T lymphocytes suggested the synthesis of IL-2 by neural cells. Lipopolysaccharide and hypoxia triggered IL-2 synthesis by cultured microglia with a peak after exposure to lipopolysaccharide and hypoxia. Double-labeling showed, in vivo and in vitro, that IL-2 immunoreactivity was colocalized with a microglia/macrophage marker. These results disclosed the ability of microglia to produce IL-2 and also suggest the implication of IL-2 in neural cell death triggered by perinatal lipopolysaccharide and hypoxia/ischemia exposures.