对于肠道丁酸盐的输送和宿主微生物相互作用的剖析来说,共生细菌的代谢工程
Xu Gong1, Hongwei Geng1, Yun Yang1
1Beijing Advanced Innovation Centre for Biomedical Engineering, Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Engineering Medicine, Beihang University, Beijing, 100191, PR China; Key Laboratory of Big Data-Based Precision Medicine, Ministry of Industry and Information Technology, Beihang University, Beijing, 100191, PR China.
Metabolic engineering
|September 17, 2023
概括
减少产生丁酸盐的肠道细菌与疾病有关. 这项研究设计了细菌来输送丁酸盐,揭示了它通过抑制大肠炎模型中的gasdermin D (GSDMD) 来保护肠道平衡.
科学领域:
- 微生物组研究的研究.
- 肠道免疫 肠道免疫是一种免疫系统.
- 主体-微生物相互作用
背景情况:
- 减少生产丁酸盐的共生类的丰富性与许多疾病相关.
- 丁酸盐在宿主粘膜免疫和病原发生中的因果作用的分子机制仍然不太清楚.
- 缺乏有效的控制肠道丁酸盐的工具,阻碍了机械学研究.
研究的目的:
- 为了设计一种细菌输送系统,用于肠道丁酸盐.
- 剖析肠道丁酸盐在调节宿主肠道平衡中的因果作用.
- 为了在老鼠慢性结肠炎模型中研究丁酸盐的机制.
主要方法:
- 设计一种可选的无氧共生细菌,用于酸盐的向输送.
- 利用慢性结肠炎的小鼠模型来评估丁酸盐的影响.
- 在结肠表皮中研究丁酸盐的分子点.
主要成果:
- 工程细菌成功地将丁酸盐输送到肠道粘膜表面.
- 肠酸表明对实验性结肠炎有保护作用.
- 丁酸盐通过抑制气体皮质素D (GSDMD),一个关键的火灭亡执行者来保持肠粘膜平衡.
- 丁酸盐作为HDAC3抑制剂起作用.
结论:
- 合成细菌可以作为活体输送载体,在宿主-微生物界面解码因果分子.
- 肠酸在维持肠道平衡中起着至关重要的作用.
- 通过丁酸盐 (通过HDAC3) 抑制GSDMD是一种保护大肠炎的关键机制.
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