鞭毛蛋白FlgE通过向ATP5B促进巨细胞激活和动脉样硬化
Yuanyuan Li1, Min Zhang1, Yanmeng Li1
1Department of Laboratory Examination, People's Hospital of Rizhao City, The Affiliated Hospital of Jining Medical College, Rizhao, China.
Atherosclerosis
|January 26, 2024
概括
Pseudomonas aeruginosa 鞭毛蛋白 FlgE 通过通过 ATP5B 信号传递增加脂肪吸收和巨细胞的炎症来促进动脉样硬化. 这澄清了将细菌感染与心血管疾病联系在一起的机制.
科学领域:
- 免疫学 免疫学 免疫学
- 心血管生物学 心血管生物学
- 微生物学 微生物学
背景情况:
- 伪菌感染与心血管疾病和动脉样硬化有关.
- 来自P. aeruginosa的鞭毛蛋白FlgE具有免疫刺激作用.
- 连接FlgE与动脉生成的机制以前尚不清楚.
研究的目的:
- 为了研究FlgE对动脉样硬化的影响.
- 阐明FlgE诱导的动脉动脉生成的潜在机制.
主要方法:
- ApoE-/-小鼠受到FlgE的挑战.
- 使用慢性肺部殖民的小鼠模型.
- 分析了THP-1巨细胞的脂质吸收和炎症.
- 西方涂抹,拉下测试和阻断实验确定了分子通路.
主要成果:
- 通过增加脂质沉积和炎症,flgE在ApoE-/-小鼠中加速动脉样硬化.
- FlgE调高了清理受体A1 (SR-A1) 的表达,加剧了脂蛋白摄取和泡细胞的形成.
- FlgE激活了巨细胞中的NF-κB和MAPK信号通路.
- FlgE与ATP5B直接相互作用,阻断ATP5B减弱了FlgE诱导的反应.
结论:
- FlgE诱导巨细胞的脂质吸收和促炎反应.
- ATP5B/NF-kB/AP-1信号通路调解了FlgE在动脉样硬化中的作用.
- 这些发现支持P. aeruginosa感染引起的动脉样硬化治疗策略.
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