Pro-inflammatory effects of aluminum in human glioblastoma cells
Pro-inflammatory effects of aluminum in human glioblastoma cells
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DOI：
10.1016/s0006-8993(02)02305-3
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发表时间：
2002-04-12
期刊：
影响因子：
2.9
通讯作者：
Bondy, SC
中科院分区：
文献类型：
--
作者：
Campbell, A;Yang, EY;Bondy, SC
炎症事件与老年斑有关，老年斑是阿尔茨海默病（AD）的病理标志之一。据信，聚集的β-淀粉样蛋白（β A）蛋白，形成这些斑块的核心。可能是引发炎症反应的原因在本研究中，铝（Al）在人类胶质母细胞瘤细胞系中引发类似炎症事件的能力进行了研究。暴露于脂多糖（LPS）或硫酸铝中6天，导致胶质母细胞瘤细胞增殖速率显著增加。两种治疗也引起免疫应答转录因子NF-κ B的激活，尽管存在时间相关的差异。分泌的细胞因子水平。白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）均通过LPS处理而增加，尽管暴露于Al降低了前者的分泌，同时升高了后者的水平。这些事件可能是由于胶质细胞的激活和随后的铝复合物或LPS的应激反应。虽然暴露于任一应激因素引起炎症标志物的刺激，但反应存在时间依赖性差异。这可能反映了细胞辨别不同应激因子的能力，从而协调了对每种免疫原不同的先天免疫应答谱。(C)2002 Elsevier Science B. V.保留所有权利。
Inflammatory events have been associated with senile plaques, one of the pathological hallmarks of Alzheimer's disease (AD). It is believed that aggregated beta-amyloid (betaA) proteins, which form the core of these plaques. may be responsible for triggering the inflammatory reaction. In the present study, the ability of aluminum (Al) to initiate similar inflammatory events was investigated in a human glioblastoma cell line. A 6-day exposure to either lipopolysaccharide (LPS) or aluminum sulfate caused a significant increase in the rate of proliferation of the glioblastoma cells. Both treatments also caused activation of the immune-responsive transcription factor NF-kappaB although there were time-related differences. The levels of secreted cytokines. interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were both increased by the LPS treatment although exposure to Al decreased the secretion of the former while elevating the levels of the latter. These events may be due to the activation of glial cells and subsequent stress response to either Al complexes or LPS. Although exposure to either stress factor caused a stimulation of inflammatory markers, there were time-dependent differences in the response. This may reflect the ability of the cells to discern different stress factors and thus orchestrate an innate immune response profile distinct to each immunogen. (C) 2002 Elsevier Science B.V. All rights reserved.