微生物组的饮食调节会影响自身炎症性疾病
John R Lukens1, Prajwal Gurung1, Peter Vogel2
1Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Nature
|October 3, 2014
概括
饮食中的脂肪和胆固醇通过改变肠道微生物组并降低介质蛋白-1β (IL-1β) 生产,保护小鼠免受炎症性骨病的影响. 这涉及Prevotella细菌和caspase-8信号传递.
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.
- 骨生物学 骨生物学 骨生物学
背景情况:
- 慢性炎症性疾病正在增加,饮食可能起作用,但机制尚不清楚.
- Pstpip2 ((cmo) 鼠会发展出类似人类慢性复发多焦点骨髓炎的骨髓炎.
- 之前的研究表明,互白素-1β (IL-1β) 的参与,但炎症组分 (caspase-1,NLRP3) 没有保护这些小鼠.
研究的目的:
- 确定控制Pstpip2 (cmo) 小鼠IL-1β生产的上游机制.
- 为了研究推动IL-1β依赖性炎症性骨质侵蚀的环境因素.
- 阐明饮食和肠道微生物群在骨髓炎发病过程中的作用.
主要方法:
- 在Pstpip2 ((cmo) 小鼠中分析肠道微生物群.
- 饮食干预 (高脂肪,高胆固醇饮食) 在pstpip2cmo小鼠中.
- 在Pstpip2 ((cmo) 和野生型小鼠中进行了抗生素治疗和无菌条件.
- 炎症体组件 (caspase-1,NLRP3) 和caspases (caspase-1,caspase-8) 的遗传删除.
主要成果:
- 患有Pstpip2 ((cmo) 病的小鼠在肠道微生物群中表现出Prevotella的外生.
- 富含脂肪和胆固醇的饮食保护小鼠免受骨质炎,减少了Prevotella和亲IL-1β表达.
- 抗生素治疗和无细菌条件也减少了亲IL-1β的表达.
- 对于对IL-1β依赖性骨病的保护,caspase-1和caspase-8的联合删除是必要的.
结论:
- 肠道微生物组与饮食相关的变化是骨质炎的关键调节者.
- 这些发现突显了一条涉及Prevotella,饮食和IL-1β通过炎症和酶-8成熟的途径.
- 这项研究揭示了饮食,肠道微生物群和IL-1β驱动的炎症性骨病之间的新联系.
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