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在基于活动的厌食症模型中,肠上皮层TLR4淘汰会对肠道屏障和微生物群产生性别特异性影响

Colin Salaün^1,2, Marion Huré^1,2, Charlène Guérin^1,2

¹INSERM, Normandie Université, ADEN UMR1073 'Nutrition, Inflammation and microbiota-gut-brain axis', Univ Rouen Normandie, Rouen, France.

|February 28, 2026

概括

诱导性托尔类受体4在肠上皮细胞中的淘汰 (TLR4^IEC^-/-) 在小鼠中引起性别特异的肠道变化. 这些肠道屏障,炎症和微生物群的变化不在基于活动的厌食症模型中.

科学领域:

微生物学微生物学
胃肠病学胃肠病学
神经科学是一个神经科学.

背景情况:

微生物群-肠-大脑轴在神经性厌食症病理生理学中发挥着作用.
在基于活动的厌食症 (ABA) 小鼠的肠上皮细胞 (IEC) 中观察到增加的托尔类受体4 (TLR4) 表达.
在IEC中诱导TLR4淘汰 (TLR4^IEC^-/-) 影响了ABA小鼠的行为和能量平衡.

研究的目的:

为了研究雄性和雌性ABA小鼠对TLR4的肠道反应.
分析炎症变化,肠道屏障完整性和肠道微生物群组成.
为了确定TLR4^IEC^-/-对肠道的性别特异性影响.

主要方法:

在IEC中诱导TLR4淘汰 (TLR4^IEC^-/-) 在雄性和雌性小鼠中确立.
小鼠接受了基于活动的厌食症 (ABA) 模型.
分析了结肠基因表达 (43个标志物通过RT-qPCR) 和肠道微生物群组成 (16S rRNA基因测序).

主要成果:

在雄性对照小鼠中,TLR4^IEC^-/-诱导了比雌性更明显的肠道变化,包括减少炎症因素和紧结蛋白.
对照TLR4^IEC^-/-的女性显示炎症标志物增加和肠道屏障相关的基因表达.
TLR4^IEC^-/-以性别特定的方式改变了肠道微生物群的组成,男性增加了Bacillota和Deltaproteobacteria,女性增加了Alcaligenaceae.
这些TLR4^IEC^-/-诱导的肠道和微生物群变化没有在ABA模型小鼠中观察到,并且被ABA规范化.

结论:

诱导性TLR4^IEC^-/-导致特定性别的结肠炎症,肠道屏障和微生物群的改变.
基于活动的厌食症模型减轻了这些TLR4^IEC-/-诱导的肠道变化.
需要进一步的研究来阐明这些性别特异性肠道反应的潜在机制.

关键词:

神经性厌食症是一种神经性厌食症.在 TLR4 中,基于活动的厌食症小鼠.肠道屏障障碍物肠道屏障障碍物肠道炎症肠道炎症我们的肠道微生物群.

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