菌根菌与宿主之间的相互作用 微粒重塑血脑屏障结合点 进行脑部入侵
Megan I Hayes1, Sumedha Ravishankar1, Jonathan K Shanahan2
1School of Biological Sciences, University of California, San Diego, La Jolla, CA 92037, USA.
Cell reports
|December 12, 2025
概括
菌根菌通过细胞外传播和在内皮上形成微殖民地来入侵大脑. 这一对于结核性脑膜炎至关重要的过程由三五巧克力和Mincle介导,并被多种Mycobacterium物种利用.
科学领域:
- 神经科学是一个神经科学.
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 结核性脑膜炎涉及两个阶段的过程:初始的脑部入侵由菌根和随后的形成Rich焦点.
- 了解最初的大脑入侵机制对于对抗这种严重形式的结核病至关重要.
研究的目的:
- 在斑马鱼幼虫中阐明初始菌根细菌入侵大脑的机制.
- 确定促进细菌进入中枢神经系统的分子相互作用.
主要方法:
- 利用透明的斑马鱼幼虫作为模型生物.
- 在体内观察到菌根菌的传播和与大脑微血管的相互作用.
- 研究了菌根细菌表面甘油脂和宿主受体的作用.
主要成果:
- 细胞外的菌根菌,而不是细胞内的菌根菌,到达大脑微血管系统.
- 菌根细菌粘附于内皮,形成微殖民地,并诱导紧密的结节重组.
- 三糖五巧克力和Mincle介导细菌进入和随后的微质感染.
- 多种Mycobacterium物种,包括M. tuberculosis,M. marinum和M. smegmatis,使用这种入侵途径.
结论:
- 结核菌引发脑膜炎是通过利用一种涉及内皮相互作用和三糖五巧克力-明克尔信号传递的祖先途径.
- 这种保存机制突显了不同菌根菌种对脑部入侵的共同脆弱性.
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