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与牙周炎相关的Fusobacterium nucleatum通过ferroptosis介导的肠道屏障破坏促进性结肠炎
Xiaoyue Zhang1,2, Shouzheng Cheng1,2, Shuze Chen1,2
1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, Sichuan, China.
细菌核通过触发细胞死亡途径铁亡,使性结肠炎 (UC) 恶化. 通过Ferrostatin-1抑制铁亡,在治疗这种牙-肠轴并发症方面显示出有前途.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 牙周炎和性结肠炎 (UC) 通过"牙-肠"轴联系在一起.
- 细菌核酸菌 (Fusobacterium nucleatum) 涉及到牙周炎和胃肠道疾病.
研究的目的:
- 调查F.核在UC病变发生中的作用.
- 探索牙周炎-UC并发症的潜在机制,包括铁亡.
主要方法:
- 德克斯硫酸盐诱导的UC和F.核诱导的牙周炎小鼠模型.
- 16S rRNA基因测序和LC-MS代谢学.
- 铁酶抑制剂 (费洛斯塔丁-1) 的使用.
主要成果:
- 在F. nucleatum中,UC严重程度恶化,膜骨损失和肠道屏障功能障碍.
- 在结肠中确定了铁灭激活,标志着特定的分子变化.
- 费罗斯塔丁-1治疗减弱了UC,恢复了肠道屏障的完整性.
结论:
- 在牙周炎-UC并发症中,F. nucleatum起到关键的调解作用.
- 在肠道屏障中激活ferroptosis是一个至关重要的机制.
- 向铁化提供了与牙周炎相关的UC的潜在治疗策略.
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