肠道微生物脂调节肠道基因表达,可以抵消抗生素治疗的影响
Xue-Song Zhang1, Yujue Wang2, Haipeng Sun3
1Center for Advanced Biotechnology and Medicine, Rutgers University.
bioRxiv : the preprint server for biology
|February 20, 2025
概括
早期接触抗生素通过改变肠道微生物在小鼠中加速1型糖尿病 (T1D). 通过便移植恢复的特定微生物产生的脂质显示出对T1D的抗炎潜力.
科学领域:
- 微生物组研究的研究.
- 免疫学 免疫学 免疫学
- 代谢的恒常化是代谢的恒常化.
背景情况:
- 肠道微生物组在维持免疫和代谢平衡方面发挥着至关重要的作用.
- 早期接触抗生素会破坏肠道微生物群,影响宿主新陈代谢,增加1型糖尿病 (T1D) 的风险.
研究的目的:
- 研究早期抗生素暴露对肠道微生物群和脂质谱的影响.
- 为了确定参与T1D病原和炎症的特定微生物产生的脂质.
- 探索这些脂质在缓解T1D发展方面的治疗潜力.
主要方法:
- 分析小鼠肠道脂质学特征.
- 传统的,无细菌的,和用抗生素治疗的小鼠之间的脂质特征的比较,有和没有切卡物质移植 (CMT).
- 用免疫和上皮细胞进行体外共同培养实验.
- 通过口服给抗生素治疗的NOD小鼠注射已识别的脂.
主要成果:
- 在小鼠肠道中鉴定了747种脂质化合物;87种微生物产生的脂质被抗生素减少,但被CMT恢复.
- 人类便脂质资料显示,在暴露于阿齐思罗米辛后,出现了显著的变化,与小鼠数据重叠.
- 确定了通过NFκB通路抑制炎症的脂.
- 口服脂在接受抗生素治疗的NOD小鼠中降低了T1D相关基因表达.
结论:
- 早期的抗生素暴露会对肠道脂质特征产生负面影响,并加速T1D.
- 微生物产生的脂质,特别是脂质,具有抗炎性质.
- 这些脂质代表了预防或治疗T1D的潜在治疗点.
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