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酒精使用障碍 (AUD) 与对细胞脂多糖挑战的增强敏感性有关

Elizabeth M Burnette^1,2, Erica N Grodin¹, Richard Olmstead^3,4,5

¹Department of Psychology, University of California at Los Angeles, Los Angeles, California, USA.

Alcohol, clinical & experimental research

|October 21, 2023

概括

患有酒精使用障碍 (AUD) 的个人表现出高水平的促炎性细胞因子,包括TNF-α和IL-6/TNF-α共同表达,无论是在休息状态下还是经过Toll-like受体4 (TLR4) 刺激后. 这项研究引入了一种新的方法来评估AUD中的免疫信号.

科学领域:

神经免疫学神经免疫学
传染性疾病传染性疾病
免疫学免疫学免疫学

背景情况:

酒精使用障碍 (AUD) 与炎症有关.
通过脂聚糖 (LPS) 刺激托尔类受体4 (TLR4) 可以揭示免疫信号.
在单细胞中研究细胞内细胞因子 (ICC) 生产提供了一种新的方法来表征AUD相关的免疫反应.

研究的目的:

评估AUD和单细胞ICC生产之间的关系.
评估休息时的ICC水平和使用LPS刺激TLR4后的ICC水平.
探索这种方法在理解AUD中神经免疫机制方面的实用性.

主要方法:

分析了36名参与者的血液样本 (14名AUD,22名对照).
评估细胞内细胞因子表达 (TNF-α,IL-6,IFN和共同表达) 在休息状态和LPS刺激后.
使用线性混合效应模型来分析数据,控制BMI和时间点,以AUD和LPS作为固定效应及其相互作用.

主要成果:

与对照人群相比,患有AUD的个体表现出TNF-α的非刺激和LPS刺激单细胞表达显著更高.
对于TNF-α和TNF-α/IL-6的共同表达,观察到显著的AUD × LPS相互作用,这表明AUD组的反应增加.
对于单独IL-6来说,没有发现AUD或LPS的显著影响,但对IL-6和TNF-α/IL-6联合表达的时间点效应被注意到. 干扰素 (IFN) 也显示出AUD,LPS及其相互作用的显著影响.

结论:

AUD与TNF-α和TNF-α/IL-6联合表达的高休息和TLR4刺激的单细胞产生有关.
这项研究提供了第一个证据,将AUD与静止状态和TLR4刺激时的单细胞亲炎性细胞因子产生联系起来.
这些发现支持AUD中促炎细胞因子的作用,并验证了一种用于AUD中探测神经免疫机制的新方法.

关键词:

酒精使用障碍饮酒障碍细胞因子细胞因子这是一种炎症炎症炎症炎症.脂多糖类糖化物 (Lipopolysaccharide) 是一种脂多糖类糖.

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