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高脂肪饮食诱导炎症性IMD/NFκB信号通过肠道微生物群重塑在Drosophila中

Jun Wang¹, Jiaojiao Gu¹, Jianhan Yi¹

¹Hunan Provincial Key Laboratory of Animal Intestinal Function and Regulation, College of Life Sciences, Hunan Normal University, Changsha, China.

Frontiers in cellular and infection microbiology

|May 8, 2024

概括

高脂肪饮食通过改变肠道细菌引发炎症. 这导致细菌分子二醇的增加,激活远程组织中的免疫反应.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
营养科学营养科学

背景情况:

高脂肪饮食 (HFD) 与慢性炎症和疾病有关.
连接HFD与炎症的机制,特别是神经炎症,需要进一步阐明.

研究的目的:

研究HFDs在偏远组织中诱导炎症的机制.
探索肠道微生物群在HFD引起的炎症中的作用.

主要方法:

使用一个 *Drosophila* 模型养高脂肪饮食.
分析了肠道微生物群的组成及其对免疫路径的影响.
研究了特定细菌物种及其产品的作用.

主要成果:

HFDs通过肠道微生物群重塑激活了头部的IMD/NFκB免疫路径.
肠道微生物群的枯竭消除了HFD诱导的远程炎症.
* Acetobacter malorum * 在HFDs上增加了丰富度,并且其重新引入引起了炎症.
通过*A. malorum*增加的糖 (PGN) 生产被确定为一个关键的调解者.

结论:

HFDs通过肠道微生物群的改变和细菌分子模式促进炎症.
来自*Acetobacter malorum*的糖是调解HFD诱导的远程炎症的关键因素.

关键词:

这种细菌是Acetobacter malorum.在IMD/NFκB中.我们的肠道微生物群.高脂肪饮食高脂肪饮食酸甘油可以是酸甘油.

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