双S暴露会通过改变肠道微生物组诱导肠道炎症
Shiqi Li1, Xuan Ma1, Xueer Zhang1
1Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China; Department of Microbiology and Infection, School of Public Health, Nanjing Medical University, Nanjing, China.
双S (BPS) 暴露会通过破坏肠道微生物群和新陈代谢,导致小鼠的肠道炎症. 抗生素治疗表明肠道微生物调解了这种BPS毒性,提供了潜在的治疗点.
科学领域:
- 环境健康 环境健康
- 微生物学 微生物学
- 毒理学 毒理学 毒理学
背景情况:
- 双S (BPS) 是食品包装中常见的双A替代品.
- 有关BPS毒性的担忧存在,但其在肠道炎症中的作用尚不清楚.
研究的目的:
- 调查肠道微生物是否调解双S (BPS) 诱导的肠道炎症.
- 阐明BPS在肠道中毒性的潜在机制.
主要方法:
- 双S (BPS) 暴露的小鼠模型.
- 16S rRNA基因测序用于肠道微生物群分析.
- 没有针对性的LC-MS/MS代谢和转录组分析.
- 用抗生素治疗,以评估肠道微生物群的作用.
主要成果:
- 暴露于BPS引起了肠道炎症 (结肠缩短,密室扭曲,亡).
- BPS改变了肠道微生物群的组成,增加了促炎性微生物,减少了抗炎性微生物.
- BPS破坏了宿主和细菌的新陈代谢,改变了肠道基因表达.
- 抗生素治疗改善了BPS诱导的炎症,证实了微生物群的参与.
结论:
- 双S (BPS) 通过改变肠道微生物群的组成和功能来诱导肠道炎症.
- 肠道微生物群在调解BPS毒性方面发挥着至关重要的作用.
- 马德卡西克酸显示出防止BPS诱导的肠道炎症的潜力.
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