鼠标对人类炎症性肠病的适应 微生物群提高殖民效率并改变微生物群的侵略性 取决于接收者结肠炎症环境
Simon M Gray1,2, Anh D Moss1,3, Jeremy W Herzog2
1These authors contributed equally to this work.
bioRxiv : the preprint server for biology
|February 8, 2024
概括
对于炎症性肠道疾病 (IBD) 的可复制的小鼠模型至关重要. 适应小鼠的人类微生物群,而不是直接便微生物群移植 (FMT),确保了IBD研究中的一致实验结果.
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:
- 可复制的小鼠模型对于研究炎症性肠道疾病 (IBD) 和肠道炎症与微生物失生症之间的相互作用至关重要.
- 人类便微生物群移植 (FMT) 到与人类微生物群相关 (HMA) 的小鼠可以引入显著的实验变异性,因为转移效率低.
研究的目的:
- 研究便微生物群转移效率对实验性结肠炎模型的影响.
- 开发一个更可复制的小鼠模型来研究人类微生物群驱动的IBD.
- 探索宿主炎症在IBD期间塑造肠道微生物群中的作用.
主要方法:
- 直接的人对老鼠的FMT与Il-10-/-小鼠中适应老鼠的人类微生物群的老鼠对老鼠转移进行了比较.
- 在接受小鼠中评估了微生物群组成和结肠炎的严重程度.
- 使用无菌 (GF) 和野生型 (WT) 鼠标来评估宿主炎症环境的特异性.
主要成果:
- 直接的人类FMT导致转移效率低,微生物群组成和结肠炎严重程度的高变化.
- 适应小鼠微生物群的小鼠对小鼠的转移产生了高效率和低变异性,使可重复性结肠炎表型成为可能.
- 与非炎症宿主 (WT) 相比,炎症宿主 (Il-10-/-) 重组了一个更具攻击性的微生物群.
结论:
- 一种新型的适应小鼠的人类微生物群模型提供了一个可复制的系统,用于研究像IBD这样的人类微生物群驱动的疾病.
- 有效的IBD管理可能需要针对宿主免疫反应和由炎症驱动的微生物群转移.
- 这个模型可以被推广到研究其他微生物群调节的疾病,如肥胖,糖尿病,自身免疫性疾病和癌症.
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