在1型糖尿病模型中,肠道微生物群和免疫系统的相互调节
Estela Rosell-Mases1, Alba Santiago2, Marta Corral-Pujol1
1Immunology and Immunopathology Group, Department of Experimental Medicine, Faculty of Medicine, Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida), 25198, Lleida, Spain.
Nature communications
|November 27, 2023
概括
具有Th17表型的转基因小鼠降低了1型糖尿病 (T1D) 的发生率. 共同住房揭示了肠道微生物群和免疫转变,表明肠道细菌与NOD小鼠T1D发育之间的联系.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 遗传学 是一个遗传学.
背景情况:
- 非肥胖糖尿病 (NOD) 鼠标模型对于研究1型糖尿病 (T1D) 是至关重要的.
- 转基因NOD小鼠 (116C-NOD) 显示Th17免疫反应和减少T1D.
- 了解免疫系统和肠道微生物群之间的相互作用是T1D病变的关键.
研究的目的:
- 研究116C-NOD Th17表型对NOD小鼠T1D发育的影响.
- 探索肠道微生物群和免疫细胞子集在调节T1D发病率中的作用.
- 阐明肠道微生物组与T1D中的宿主免疫之间的相互相互作用.
主要方法:
- 在同居条件下对NOD和116C-NOD小鼠T1D发病率进行比较分析.
- 评估肠道微生物群组成,肠道透性和免疫细胞 (T和B细胞) 配置文件.
- 使用RAG-2淘汰赛小鼠模型 (NOD.RAG-2-/-和116C-NOD.RAG-2-/-) 来研究T细胞依赖的微生物变化.
主要成果:
- 同住116C-NOD小鼠和NOD小鼠减少了NOD小鼠的T1D发病率,与改变的肠道微生物群相关,肠道透率降低,并从Th1到Th17反应转移.
- 在每个小鼠组中,不同的肠道细菌特征与T1D有关.
- T细胞的改变促进了细分丝状细菌 (SFB) 的增殖,而Bifidobacterium的殖民是淋巴细胞依赖的,有利于非糖尿病的环境.
- 免疫缺陷小鼠中的116C-NOD B细胞丰富了Adlercreutzia和降低了肠道透性.
结论:
- 肠道微生物群和免疫系统之间的相互调制在动物模型中显著影响T1D的发展.
- Th17表型和特定的肠道细菌,如Adlercreutzia,在T1D中起着保护作用.
- 免疫细胞子集关键调节肠道微生物的组成和功能,影响肠道屏障的完整性.
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