比菲多细菌infantis调节肠道微生态,以抑制抗菌素耐药性的传播
Ziyun Li1,2, Jiamin Hu3, Yingmiao Pan1
1Microbiome-X, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
mSystems
|October 31, 2025
概括
补充Bifidobacterium infantis通过增强胆汁酸和抑制耐药细菌,减少了小鼠抗生素耐药性基因的传播. 这种益生菌干预提供了一种打击抗微生物耐药性 (AMR) 和保护肠道健康的新策略.
科学领域:
- 微生物学和肠道健康
- 抗微生物耐药性 (AMR) 机制
- 益生菌和肠道微生物群的调节
背景情况:
- 儿童早期使用抗生素增加了对多抗药性感染的易感性.
- 益生菌在抑制抗菌素耐药性 (AMR) 和抗生素耐药性基因 (ARG) 传播中的作用尚未完全理解.
- 由于过度使用抗生素导致肠道微生物群的不平衡,增加了ARG水平基因转移的风险.
研究的目的:
- 研究Bifidobacterium infantis在抑制肠道内抗生素耐药性基因 (ARG) 传播中的作用.
- 阐明B. infantis调节肠道环境以减少ARG传播的机制.
- 为针对AMR的新型益生菌干预提供理论基础.
主要方法:
- 在小鼠中使用Bifidobacterium infantis 15697.7的补充剂.
- 对肠道微生物群组成,胆酸合成和ARG丰度的分析.
- 利用小鼠感染模型评估B. infantis对抗生素耐药性大肠杆菌殖民和水平基因转移的影响.
主要成果:
- 补充B. infantis显著增加了胆酸合成 (TUDCA,TCA) 和大量有益的益生菌,如Parabacteroides goldsteinii.
- B. infantis 抑制了抗生素耐药的大肠杆菌的殖民,并减少了水平基因转移事件,从而减少了ARG传播.
- 通过与OmpC蛋白相互作用,发现tauroursodeoxycholic acid (TUDCA) 和taurocholic acid (TCA) 抑制了生物膜的形成,并降低了抗生素耐药细菌的细胞膜透性.
结论:
- 双杆菌 (Bifidobacterium infantis) 在调节肠道微生物群和抑制抗生素耐药性基因 (ARG) 传播方面发挥着至关重要的作用.
- 该机制涉及胆酸代谢的调节,特别是TUDCA和TCA,这些直接阻碍了抗生素耐药细菌.
- B. infantis代表了一种有前途的益生菌战略,用于减少抗药性耐药性,保护儿童和成人肠道健康,并为公共卫生政策提供信息.
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