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肠道LGR4信号改变了细菌转位,肝内微生物群组成和1型干扰素表达在小鼠肝纤维化中的表达

Junyan Gao¹, Bangtao Chen², Cheng Chen³

¹Department of Basic Medicine, Changzhi Medical College, Changzhi, 046000, China.

|December 20, 2025

概括

肠道LGR4信号减弱会通过增加肠道透性和改变肝脏微生物群,使肝纤维化 (LF) 恶化. 恢复乳杆菌水平和增加1型干扰素 (IFN1) 可以帮助治疗肺炎.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
微生物学微生物学

背景情况:

肝纤维化 (LF) 与降低的1型干扰素 (IFN1) 和肠道失调有关.
肠道LGR4信号传递对于维持肠道平衡和干细胞至关重要.

研究的目的:

研究肠道LGR4信号在肝纤维化中的作用.
探索肠道LGR4,肝内微生物群和LF中的IFN1水平之间的关系.

主要方法:

碳四化物 (CCL4) 诱导了小鼠的LF,在肠道上皮细胞 (IEC) 中Lgr4的有条件淘汰 (cKO) 或没有条件淘汰.
在Lgr4 cKO小鼠中使用了Lactobacillus的胃内给药.
分析了肝脏内微生物群和IFN1水平.

主要成果:

在LF小鼠中,肠道LGR4的降低与肠道透性增加,细菌转位以及肝脏内IFN1.1的降低相关.
IECs中的Lgr4 cKO加剧了LF,改变了肝脏内微生物群的组成.
在Lgr4 cKO小鼠中,Lactobacillus的使用减弱了LF,恢复了IFN1水平,这种影响取决于IFN1受体.

结论:

肠道LGR4信号减弱通过破坏肠道屏障功能和改变肝肠轴来促进LF.
肠道LGR4信号影响肝内微生物群和IFN1的产生.
针对肠道微生物群,特别是乳酸菌,可以通过调节IFN1反应来为LF提供治疗策略.

关键词:

肠道上皮细胞肠道上皮细胞肝内微生物群肝内微生物群牛乳杆菌 (Lactobacillus) 是一种细菌.含有g蛋白结合受体4的氨酸丰富的重复物.肝脏纤维化肝脏纤维化第1型干扰素干扰素

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