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利法西明通过调节肠道微生物群来改善流感A病毒感染引起的肺障碍损伤

Yijia Zhang¹, Yafei Chen¹, Jun Xia²

¹Laboratory of Animal Neurobiology, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China.

Applied microbiology and biotechnology

|September 19, 2024

概括

利法西明治疗有助于修复由流感A病毒引起的肺损伤,通过恢复肠道微生物群平衡和促进激活免疫细胞的托芬代谢. 这种机制涉及AHR/STAT3/IL-22途径的肺屏障恢复.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

肠肺轴突出了肠道微生物群与肺免疫之间的联系.
甲型流感病毒 (IAV) 感染会破坏肠道微生物群的平衡,影响肺部健康.
利法西明是一种广泛的抗生素,可以调节肠道微生物群.

研究的目的:

在小鼠模型中调查rifaximin是否可以改善IAV诱导的肺损伤.
探索IAV感染期间利法西明对肠肺轴的影响背后的分子机制.

主要方法:

建立了感染IAV的小鼠模型,并没有补充利法西明.
分析肺部和肠道组织结构,肠道微生物群组成 (16S rRNA) 和便代谢学.
评估免疫细胞群 (ILC3),细胞因子水平 (IL-22) 和蛋白质表达 (RORγ,STAT-3,AHR,IDO-1,紧密结合蛋白).

主要成果:

IAV感染导致了显著的体重减轻,肺和肠道结构损伤,并减少了有益的肠道细菌和托代谢物.
利法西明治疗逆转了这些影响,改善了肺障碍修复,增加了特定的肠道细菌 (Muribaculum, Papillibacter),并恢复了托代谢物.
利法西明增强了ILC3细胞数量,IL-22水平,以及肺和肠道中的AHR/STAT3通路激活,减轻了屏障损伤.

结论:

利法西明通过恢复肠道微生物群的平衡和促进托代谢来缓解IAV诱导的肺损伤.
托芬作为一个信号分子,通过AHR/STAT3/IL-22通路促进ILC3细胞从肠道迁移到肺部.
利法西明的这种途径激活有助于在IAV感染后恢复肺屏障功能.

关键词:

肠肺轴肠肺轴肠肺轴在 ILC3 细胞中.流感是一个病毒病毒.里法克斯小小的时间.托芬代谢的代谢方式

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