主体和肠道密码居住生物膜之间的相互作用是由表皮化化控制的
Xue-Kun Guo1, Jiali Wang1, Vincent P van Hensbergen1
1Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing 100084, China; Beijing Key Laboratory for Immunological Research on Chronic Diseases, Tsinghua University, Beijing 100084, China.
Cell reports
|July 5, 2023
概括
主体上皮层的化抑制了肠道生物膜的形成,防止大肠炎期间的炎症恶化. 富可的使用显示了对生物膜相关疾病的治疗潜力.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 细菌生物膜与炎症有关.
- 在复杂组织中体内宿主生物膜相互作用的理解很少.
研究的目的:
- 在早期结肠炎中调查宿主生物膜相互作用.
- 确定生物膜受宿主因素限制的机制.
主要方法:
- 肠道组织的显微镜分析.
- 对细菌和宿主进行遗传操纵.
- 在体外和体内生物膜测定.
- 在实验性结肠炎中使用fucose.
主要成果:
- 粘液相关的生物膜在早期结肠炎中独特地占据了密室.
- 主体上皮层α1,2-fucosylation在遗传上限制了生物膜的形成.
- 化缺陷加剧了结肠炎,原因是菌Typhimurium和大肠杆菌生物膜增加了密室的占用.
- 糖在体外和体内抑制生物膜的形成.
- 福科斯的使用改善了实验性结肠炎.
结论:
- α1,2-Fucosylation 是对肠道生物膜形成的宿主防御机制.
- 糖作为一个信号分子来抑制生物膜的发展.
- 富可糖对与生物膜相关的炎症性疾病具有治疗潜力.
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