EgCF通过影响糖解路径来调解巨细胞的两极分化
Yeye Feng1,2, Junying Xu1,2, Junxia Lu1,2
1NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, the First Affiliated Hospital, Shihezi University School of Medicine, Shihezi, Xinjiang, China.
Journal of helminthology
|December 21, 2023
概括
人类囊性赤道球菌病 (CE) 涉及M2巨细胞的升高,这对肝纤维化至关重要. Echinococcus granulosus 囊液 (EgCF) 通过抑制缺氧诱导因子1-alpha (HIF-1α) 来驱动这种M2两极分化,从而抑制糖解.
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 分子生物学分子生物学
背景情况:
- 人类囊性乙球菌病 (CE) 是由乙球菌粒状幼虫引起的寄生性动物病,主要影响肝脏和肺部.
- 肝脏CE中M2巨细胞水平升高与肝纤维化相关,但巨细胞两极分化的潜在机制尚不清楚.
研究的目的:
- 调查埃奇诺科克菌粒状囊液 (EgCF) 诱导巨细胞偏向M2表型的机制.
- 阐明缺氧诱导因子1-alpha (HIF-1α) 在EgCF介导的巨细胞两极分化和糖解中的作用.
主要方法:
- 巨细胞培养物用EgCF.被治疗.
- 分析了M2巨标记物,抗炎细胞因子,HIF-1α和糖解相关基因 (HK2,PKM2) 的表达水平.
- 评估了HIF-1α激动剂 (ML228) 对EgCF诱导的M2极化的影响.
主要成果:
- EgCF治疗显著增加了M2巨细胞的表达和抗炎细胞因子的产生.
- EgCF抑制了HIF-1α的表达,导致糖解基因HK2和PKM2.2的表达增加.
- 通过ML228抑制HIF-1α抵消了EgCF诱导的M2极化.
结论:
- Echinococcus granulosus通过抑制HIF-1α表达来抑制巨细胞糖解.
- 这种机制有助于观察到的人类囊性赤道球菌病的M2巨分化.
- 准HIF-1α通路可能为CE提供治疗策略.
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