来自E.coli的细胞膜蛋白MipA 尼斯尔1917能防止沙门氏菌感染
Yunqing Xiang1,2, Huipai Peng1, Yanxia Li3
1State Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
结合性大肠杆菌尼斯尔1917 (EcN) 通过重塑肠道内来预防沙门氏菌感染. 一种特定的EcN蛋白MipA增强了上皮防御,提供了对抗肠道感染的新策略.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 肠道微生物群赋予了对病原体的殖民抵抗力,主要是通过直接竞争.
- 在重新塑造宿主上皮以抵抗殖民化的过程中,初生的作用较少被理解.
研究的目的:
- 通过改变宿主上皮位,研究共生细菌是否可以增强殖民抵抗力.
- 阐明大肠杆菌尼斯尔1917 (EcN) 对沙门氏甲型菌 (STm) 感染进行保护的分子机制.
主要方法:
- 在体内小鼠模型和肠上芯片系统被使用.
- 研究了EcN前殖民化在赋予对STm的耐药性的作用.
- 确定了关键的微生物因素和参与保护作用的宿主途径.
主要成果:
- 埃克尼的前殖民是对抗性传染病感染的抗性至关重要的.
- 确定了EcN外膜蛋白MipA对保护至关重要.
- MipA诱导了整合因子结合激酶 (ILK) 的上调,增强了上皮质紧密结合完整性.
- 用MipA设计一种非保护性细菌菌株,使其对STm产生抗性.
结论:
- 连体细菌可以通过重塑宿主上皮提供殖民抵抗力.
- 来自EcN的益生菌蛋白MipA增强了表皮屏障功能,限制了沙门氏菌.
- 这一发现对开发针对肠道感染的新型预防策略有影响.
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