长长的Bifidobacterium 抑制了与牙上皮质ferroptosis相关的Aggregatibacter actinomycetemcomitans,并保护细胞结点
Xiaojiao Sun1,2,3, Zehui Wang4, Dan Qiu3
1Department of Oral and Maxillofacial Surgery, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Journal of oral microbiology
|December 24, 2025
概括
双细菌 (Bifidobacterium longum,BL) 通过调节铁亡来保护牙细胞免受Aggregatibacter actinomycetemcomitans (Aa) 引起的损伤. 蓝牙保护了上皮屏障的功能,并减少了炎症,显示了牙周炎治疗的希望.
科学领域:
- 口腔微生物学 口腔微生物学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 牙周病原体破坏了牙上皮质屏障.
- 连接结节损伤,铁亡和炎症的分子机制尚未完全理解.
研究的目的:
- 为了确定Bifidobacterium longum (BL) 是否能够抵消人类牙上皮细胞 (HGEC) 中Aggregatibacter actinomycetemcomitans (Aa) 诱导的结节损伤.
- 研究铁灭菌调节在这个过程中的作用.
主要方法:
- 16S rRNA测序和口腔微生物群的生物信息学分析.
- 暴露于HGECs的Aa和BL或ferrostatin-1 (Fer-1) 的治疗.
- 评估细胞活力,线粒体形态,活性氧物种 (ROS),结蛋白,铁灭菌标志物和炎症性细胞因子.
主要成果:
- Aa诱导线粒体损伤,ROS积累,并抑制保护性铁亡信号和结合蛋白,导致炎症失衡.
- BL治疗恢复了线粒体的完整性,铁亡信号传递,上皮结和炎症平衡.
- BL的效果与Fer-1.1的效果相似或更大.
结论:
- 聚聚细菌actinomycetemcomitans通过铁质中介的氧化和炎症损伤破坏牙上皮质的完整性.
- Bifidobacterium longum有效地抑制了这一过程,保护了上皮结,并为牙周炎提供了治疗潜力.
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