盖莱克-3促进了海利哥巴克特杆菌诱导的亡,而不需要感知溶解体损伤
Yu-Hsien Hung1,2, Fang-Yen Li1,3, Huang-Yu Yang2,4
1Institute of Biomedical Sciences, Academia Sinica, No. 128, Sec. 2, Academia Rd., Nangang Dist., Taipei 115201, Taiwan.
Glycobiology
|November 24, 2025
概括
杆菌感染促进了上皮细胞的死亡,通过在受损的溶解体周围诱导加勒-3的积累. 这种宿主因子, galectin-3,通过蛋白相互作用驱动细胞亡,独立于O-甘氨酸结合,并与自开始有关.
科学领域:
- 微生物学 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:
- 杆菌是一种常见的胃病原体,与胃炎,和癌症有关.
- 加列-3在免疫反应和细胞死亡中起作用,但在H. pylori感染期间其功能尚未完全理解.
研究的目的:
- 为了研究甲状腺细胞在H. pylori感染期间对甲状腺素-3在上皮细胞命运中的作用.
- 阐明加勒-3在对H. pylori的反应中影响亡的机制.
主要方法:
- 使用了AGS上皮细胞和加勒-3淘汰细胞.
- 使用显微镜观察了在受损的溶酶体周围的加勒-3局部化.
- 评估了亡和自的标志物 (LC3).
- 使用药理上抑制了加勒-3糖结合的作用.
主要成果:
- H.pylori 感染导致细胞溶解性 galectin-3 在受损的 lysosomes 周围积累,需要 O-glycan.
- 加列-3表达与感染诱导的亡相关,独立于VacA.
- 抑制加勒-3甘氨酸结合阻断了 lysosomal puncta,但没有细胞亡,这表明蛋白质-蛋白质相互作用介导细胞死亡.
- 盖莱克-3点点与自细胞共定位,自细胞的启动促进了亡.
结论:
- 盖莱克-3在表皮细胞对H. pylori的反应中起到前亡的作用.
- 盖莱克-3通过糖独立相互作用促进细胞亡.
- 自与促进H. pylori诱导的上皮细胞死亡有关.
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