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益生菌细菌释放的细胞外囊泡通过激活FPR1/2通路来增强多微生物性败血症中的巨细胞消化

Ruiyao Zhu^1,2,3, Yu Zhang², Xiaohong Wang²

¹Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Molecular medicine (Cambridge, Mass.)

|November 15, 2024

概括

益生菌细菌释放的细胞外囊泡 (BEVs) 增强巨细胞化,以清除败血症中的细菌. 来自戈尔巴赫-戈尔丁的Lactobacillus rhamnosus BEVs (BEV^LGG) 显示出对败血症引起的器官损伤和死亡的治疗潜力.

科学领域:

微生物学和免疫学
细胞外囊泡细胞外囊泡
败血症病理生理学病理生理学

背景情况:

败血症死亡率与细菌清除受损和器官衰竭有关.
益生菌细菌释放的细胞外囊泡 (BEVs) 调节炎症,但它们在败血症 fagocytosis 中的作用尚不清楚.

研究的目的:

为了研究BEVs在败血症期间巨细胞灭菌的功能作用.
在败血症模型中评估特定BEVs的治疗潜力.

主要方法:

在不同的pH条件下从Lactobacillus rhamnosus Gorbach-Goldin (LGG) 和其他益生菌中收集的BEV.
在实验室中使用大肠杆菌生物颗粒评估巨细胞化.
在多微生物败血症模型中评估BEVs的体内治疗效果.

主要成果:

来自LGG的BEVs (BEV^LGG),特别是那些来自性pH8培养 (BEV^pH8) 的BEVs,显著增强了巨细胞化.
在败血症小鼠中,BEV^pH8治疗延长了生存时间,增加了细菌清除,减少了炎症和器官损伤.
在机械上,BEV^pH8激活了巨细胞中的FPR1/2信号传递,PI3K-Akt-MARCO和NADPH-ROS通路,这些通路对细胞形成至关重要.

结论:

来自LGG的BEV通过FPR1/2信号增强了巨细胞化.
BEV^LGG,特别是BEV^pH8,证明了对败血症引起的器官损伤和死亡的治疗疗效.

关键词:

细胞外囊泡中的细胞外囊泡.这是FPR1/2信号.巨细胞的细胞化.益生菌 Lactobacillus rhamnosus GG GG 的使用方法败血症这是一种败血症.

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