Expression of interleukin-17 in ischemic brain tissue
Expression of interleukin-17 in ischemic brain tissue
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DOI：
10.1111/j.1365-3083.2005.01683.x
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发表时间：
2005-11-01
影响因子：
3.7
通讯作者：
Li, HL
中科院分区：
文献类型：
--
作者：
Li, GZ;Zhong, D;Li, HL
缺血性脑损伤是急性局部炎症，导致促炎细胞因子的积聚。细胞因子影响白细胞的募集并在炎症损伤过程中起关键作用。近年来，大量研究表明脑缺血与脑损伤有着密切的关系。和细胞因子。白细胞介素-17（IL-17）是一种新发现的T细胞特异性细胞因子。在这项研究中，我们评估了IL-17在大鼠（Sprague-Dawley）和人类脑缺血过程中的来源和作用。采用免疫组织化学方法检测尸检时取出的人脑缺血半球中IL-17的水平。在大鼠中，通过将尼龙单丝插入右侧颈外动脉，闭塞右侧大脑中动脉，获得永久性大脑中动脉闭塞（pMCAO）。用寡核苷酸探针原位杂交法检测大鼠IL-17 mRNA的表达。通过使用抗体胶质细胞酸性蛋白（GFAP）和抗体IL-17的双重染色来测定神经胶质细胞的IL-17产生。IL-17的水平在人脑的缺血半球中与相对的正常半球相比升高，并且在脑缺血后3-5天达到峰值。IL-17阳性细胞分布于缺血区。IL-17 mRNA在pMCAO手术大鼠的缺血半球中也升高，其在1 h后略有升高，并在6 d达到峰值。IL-17和GFAP双染在大鼠缺血半球广泛存在。本文首次报道了脑缺血诱导的人脑IL-17表达与大鼠脑缺血诱导的IL-17表达非常相似，只是峰值稍早。我们首次发现IL-17参与了人脑缺血损伤的强烈炎症反应。在pMCAO手术的大鼠中，我们的研究结果表明，IL-17是由大脑区域中的神经胶质细胞产生的缺血性损伤。我们认为，除了T细胞的神经胶质细胞可能是另一个细胞来源的IL-17在脑缺血后期进展。
Ischemic brain injury is acute local inflammation, leading to accumulation of pro-inflammatory cytokines. Cytokines influence the recruitment of leucocytes and play a key role in the inflammatory injury processes. Recently, a number of studies have demonstrated a close relationship between brain ischemia. and cytokines. Interleukin-17 (IL-17) is a newly identified T-cell-specific cytokine. In this study, we evaluated the source and the action of IL-17 over the course of cerebral ischemia in rats (Sprague-Dawley) and humans. The levels of IL-17 in the ischemic hemisphere of the human brain, which was removed at necropsy, were assayed immunohistochemically. In rats, permanent middle cerebral artery occlusion (pMCAO) was obtained by inserting nylon monofilament into the right external carotid artery, occluding the right middle cerebral artery. The expression of IL-17 mRNA in rat was assayed using oligoprobe in situ hybridization. IL-17 production by neuroglial cells was assayed by double-staining using antibody glial fibrillary acidic protein (GFAP) and antibody IL-17. Levels of IL-17 were elevated in the ischemic hemispheres of human brain compared with the opposite normal hemispheres and peaked at days 3-5 after brain ischemia. The IL-17-positive cells were found in the ischemic lesion region. IL-17 mRNA was also elevated in ischemic hemispheres of pMCAO-operated rats, which were slightly elevated after 1 h and peaked at 6 days. IL-17 and GFAP double-stained were extensive in rat ischemic hemisphere. The ischemia-induced IL-17 expression in human brain reported here for the first time was very similar to that in rat model except that the peak was slightly earlier. We found for the first time that IL-17 was involved in an intense inflammatory reaction of brain ischemic injury in human. In pMCAO-operated rats, our findings suggest that IL-17 is produced by the neuroglial cells in the brain region undergoing ischemic insult. We suggest that in additional to T cells the neuroglial cell may be another cellular origin of IL-17 in later progression of brain ischemia.