与感染相关的胆酸干扰有助于肝硬化患者的巨细胞激活
Yong Su1, Qiaoling Zhou1, Qiong Wu1
1School of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Molecular medicine reports
|July 4, 2024
概括
肝硬化患者的感染会改变胆酸概况,减少氧化胆酸 (HDCA) 和脱氧化胆酸 (DCA). 这些减少的胆汁酸在暴露于脂多糖 (LPS) 时会使巨细胞功能障碍恶化.
科学领域:
- 肝病学和免疫学 肝病学和免疫学
- 微生物学与传染病的研究
背景情况:
- 肝硬化会破坏胆酸平衡,并损害巨细胞的功能.
- 感染对胆酸概况和随后肝硬化中巨细胞功能的影响尚不清楚.
研究的目的:
- 为了调查肝硬化患者感染的胆汁酸概况的变化.
- 为了确定感染改变胆汁酸对巨细胞功能的影响.
主要方法:
- 使用高性能液态染色学-三倍飞行时间质谱学分析了血清胆汁酸概况.
- 宏细胞功能 (迁移,细胞,炎症标志物) 在体外评估,使用受感染改变的胆汁酸和脂多糖 (LPS) 刺激的细胞系.
- 接收器操作特征 (ROC) 曲线分析确定了与感染相关的关键胆酸.
主要成果:
- 降低氧胆酸 (HDCA) 和脱氧胆酸 (DCA) 的水平与肝硬化患者的感染有很强的关联.
- HDCA和DCA与LPS结合,增强了巨细胞的细胞和迁移能力,上调iNOS,CD86,TNFα,IL1β和IL6.
- 这些胆汁酸协同增加了LPS诱导的p-IκBα表达和p65核转位,表明增强了炎症信号.
结论:
- 感染显著改变肝硬化中的胆酸概况,其特征是HDCA和DCA水平降低.
- 降低的HDCA和DCA水平在对LPS的反应中加剧了巨细胞功能障碍,这表明在感染易感性方面发挥了作用.
- 监测胆汁酸概况可能有助于管理肝硬化和感染患者.
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