首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >beta-Amyloid induces increased release of interleukin-1 beta from lipopolysaccharide-activated human monocytes.
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beta-Amyloid induces increased release of interleukin-1 beta from lipopolysaccharide-activated human monocytes.

机译:β-淀粉样蛋白诱导脂多糖激活的人单核细胞释放白介素-1β的释放增加。

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摘要

Previous reports have demonstrated that IL-1 is elevated in the Alzheimer's disease brain. We propose that beta-amyloid (A beta) in senile plaques triggers microglial interleukin-1(IL-1) release. Since microglia and monocytes have similar lineage and functions, the human monocyte cell line, THP-1, was used to determine whether A beta peptides can stimulate release of IL-1 beta. THP-1 cells were grown in culture with LPS and incubated with various A beta peptides (0.5-10 microM). IL-1 released into the medium was measured using either an IL-1 beta ELISA or an IL-1 bioassay. Treatment of activated THP-1 cells with A beta 25-35, fibrillar A beta 1-40, or A beta 1-42 significantly elevated IL-1 beta release. A beta 25-35 with a scrambled sequence or non-fibrillar A beta 1-40 did not significantly change IL-1 beta release from activated THP-1 cells. The A beta 25-35- and fibrillar A beta 1-40 induced IL-1 beta release was dose-dependent. IL-1 released following treatment with A beta 25-35 and measured usingan IL-1 bioassay gave similar results. The present report provides evidence that A beta is capable of elevating release of functional IL-1 beta, a potent pro-inflammatory cytokine, from macrophages/microglia and provides support that a chronic local inflammatory response is an ongoing phenomenon within and surrounding senile plaques.
机译:先前的报道表明,阿尔茨海默氏病脑中IL-1升高。我们建议老年斑中的β-淀粉样蛋白(A beta)触发小胶质白细胞介素1(IL-1)释放。由于小胶质细胞和单核细胞具有相似的谱系和功能,因此人类单核细胞系THP-1用于确定Aβ肽是否可以刺激IL-1β的释放。 THP-1细胞在LPS培养中生长,并与各种Aβ肽(0.5-10 microM)孵育。使用IL-1βELISA或IL-1生物测定法测量释放到培养基中的IL-1。用A beta 25-35,原纤维A beta 1-40或A beta 1-42处理活化的THP-1细胞可显着提高IL-1 beta释放。具有混乱序列或非原纤维A beta 1-40的beta 25-35不会显着改变激活的THP-1细胞的IL-1 beta释放。 Aβ25-35和原纤维Aβ1-40诱导的IL-1β释放是剂量依赖性的。用A beta 25-35处理后释放的IL-1并使用IL-1生物测定法测量得出的结果相似。本报告提供了证据,表明A beta能够提高巨噬细胞/小胶质细胞功能性IL-1 beta(一种有效的促炎细胞因子)的释放,并支持慢性局部炎症反应是老年斑内和周围的持续现象。

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