Porphyromonas gingivalis 劫持 mitophagy 和 lysosomal 功能 在内皮细胞中持续存在
Cheng Zheng1, Jianmin Huang1, Shengming Xu1
1Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Frontiers in cellular and infection microbiology
|August 27, 2025
概括
Porphyromonas gingivalis 劫持了细胞和损害了内皮细胞中的 lysosomal 功能. 这一过程促进了细菌的存活,并可能导致动脉样硬化的发展.
科学领域:
- 细胞生物学
- 微生物学
- 病变发生
背景情况:
- Porphyromonas gingivalis (P. gingivalis) 是牙周病的关键病原体,与动脉样硬化有关.
- 虽然非选择性自有助于P. gingivalis在内皮细胞中的存活,但选择性自的作用尚不清楚.
- 这项研究探讨了P. gingivalis对细胞和溶酶体进行细胞内持久性的操纵.
研究的目的:
- 调查P. gingivalis是否会劫持 mitophagy 和 lysosomes 在内皮细胞内持续存在.
- 在选择性自的背景下阐明P. gingivalis细胞内生存的机制.
主要方法:
- 人类大动脉内皮细胞 (HAEC) 感染P. gingivalis.
- 使用西式斑点,免疫光和电子显微镜分析菌.
- 通过阿克里丁色染色,溶解感应染色和西部斑点染色来评估溶解体功能.
- 使用抗生素保护试验和SYTO-9染色的P. gingivalis存活率的评估.
主要成果:
- P. gingivalis 触发了PINK1-帕金基介导的线粒,破坏了自/线粒流.
- 观察到溶酶体功能障碍,包括溶酶体数量增加和酸度下降.
- 通过启动线粒细胞和 lysosomal 功能受损,增强了 P. gingivalis 的存活率.
- 线粒细胞活化抑制了外细胞的形成和与溶酶体的融合.
结论:
- 在内皮细胞中,P. gingivalis通过启动细胞和损害 lysosomal 功能来促进其生存.
- 这种机制抑制了异菌体的形成和降解,有助于细菌的持久性.
- 这些发现提供了关于P. gingivalis病变及其在动脉样硬化中的作用的见解.
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