肠道微生物共同加剧脊髓的炎症
Eiji Miyauchi1, Seok-Won Kim1, Wataru Suda1
1RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Nature
|August 28, 2020
概括
肠道微生物在多发性硬化症 (MS) 中起作用. 两种特定的肠道细菌菌株协同激活T细胞, 在小鼠中恶化MS症状,
科学领域:
- 微生物学
- 免疫学
- 神经科学
背景情况:
- 肠道微生物越来越多地与多发性硬化症 (MS) 等自身免疫性疾病有关.
- 肠道微生物在MS中影响肠外炎症的确切机制尚不清楚.
研究的目的:
- 阐明肠道微生物是如何导致多发性硬化症的.
- 识别特定的肠道微生物信号, 激活自身反应性T细胞.
主要方法:
- 在小鼠中诱导实验性自身免疫脑炎 (EAE).
- 用特定的肠道细菌对无细菌小鼠进行单一殖民.
- 精细肠道的排序.
- 对MOG特异性CD4+T细胞反应的分析.
主要成果:
- 患有EAE的小鼠在小肠中显示了MOG特异性的CD4+T细胞.
- 一种新的Erysipelotrichaceae菌株增强了T辅助细胞的反应,作为辅助剂.
- 一种Lactobacillus reuteri菌株具有模仿MOG的.
- 与单一殖民或无菌的小鼠相比,与两种菌株共同殖民加剧了EAE症状.
结论:
- 两种不同的肠道微生物信号协同激活小肠中的自反应性T细胞,从而导致MS的发病.
- 这些发现突显了特定肠道细菌在MS严重性的作用.
- 针对这些微生物相互作用可能为多发性硬化提供新的预防策略.
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