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脂多糖对能量代谢和免疫细胞激活在不同的微质模型系统的影响

Susanne Michels¹, Johanna Eichberg², Fahd Alhamdan³

¹Institute of Pharmacology and Clinical Pharmacy, University of Marburg, Marburg, Germany; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.

Brain, behavior, and immunity

|January 6, 2026

概括

微质代谢在物种和模型之间有所不同. 糖解是激活和释放细胞因子的关键,但氧化是氧化的关键.

科学领域:

神经免疫学神经免疫学
细胞的新陈代谢

背景情况:

微质细胞是关键的脑免疫细胞,对像脂聚糖 (LPS) 这样的刺激做出反应.
激活涉及代谢转移和媒介释放,但物种和模型系统的差异很大.
了解这些变异是神经疾病治疗的关键.

研究的目的:

为了比较人类和动物微质模型中LPS诱导的代谢和氧化 (NO) 生产差异.
研究NO在微质代谢重编程和促炎反应中的作用.

主要方法:

动物 (BV-2细胞系) 和人类 (iPSC衍生) 微质模型的比较分析.
评估LPS刺激后的代谢变化 (糖解,氧化酸化) 和NO产量.
诱导性氧化合成酶 (iNOS) 表达和细胞因子释放的评估.

主要成果:

鼠BV-2细胞显示与糖解相关的NO生产,并阻断了氧化酸化.
人类iPSC衍生的微质细胞和老鼠微质细胞维持了线粒体呼吸,并且具有最小的NO/iNOS.
对于LPS诱导的糖解或促炎性细胞因子释放,NO并不重要.

结论:

糖解对于微质激活和细胞因子的产生至关重要,独立于NO.
在物种和实验条件之间存在代谢途径的变化.
准确的建模对于开发有针对性的微质治疗非常重要.

关键词:

能量代谢能量代谢葡萄糖溶解是什么? 葡萄糖溶解可以诱导的氧化合成酶 (iNOS)脂聚糖化物 (LPS) 是一种微质细胞中的微质细胞线粒体呼吸线粒体呼吸支持炎症的细胞因子

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