益生菌DNA通过诱导上皮细胞产生PD-L1来调节肠道Th2极化
Shuo Song1,2, Hanqing Zhang2, Le Liu2
1Department of General Practice Medicine, Third Affiliated Hospital, Shenzhen University and State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China.
Apoptosis : an international journal on programmed cell death
|December 5, 2024
概括
乳杆菌rhamnosus (LR) DNA,而不是活益生菌,可以降低Th2免疫反应. LR-DNA在肠道细胞中增强编程细胞死亡联体-1 (PD-L1),促使Th2细胞死亡并缓解食物过敏症状.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 胃肠病学 胃肠病学
背景情况:
- Th2极化是免疫疾病的核心,但其机制需要进一步研究.
- 益生菌以其免疫调节特性而闻名.
- 了解特定的益生菌成分如何影响免疫反应至关重要.
研究的目的:
- 为了研究Lactobacillus rhamnosus (LR) DNA对Th2极化的影响.
- 阐明LR DNA免疫调节的潜在分子机制.
- 在Th2介导条件下评估LR DNA的治疗潜力.
主要方法:
- 在小鼠中使用卵白蛋白加协议确立了Th2极化.
- 每天给小鼠注射LR DNA,并评估编程细胞死亡对象-1 (PD-L1) 的表达.
- 利用RT-qPCR,ELISA,免疫组织化学和RNA测序来分析基因表达和蛋白质水平.
- 在体外测试了LR DNA对T84细胞的影响.
- 在食物过敏小鼠模型中评估了LR DNA的疗效.
主要成果:
- 在小鼠肠道上皮细胞和T84细胞中,LR DNA的使用上调了PD-L1的表达.
- RNA测序显示,LR DNA上调了Kdm5a,foxo1和Pdl1基因的活动.
- 通过与PD-1的相互作用,在激活的Th2细胞中诱导了来自表皮细胞的PD-L1诱导的亡.
- 与活益生菌不同的是,LR DNA在食物过敏模型中缓解了实验Th2极化.
结论:
- LR DNA 刺激肠道上皮细胞产生 PD-L1.1.
- PD-L1诱导激活的Th2细胞的亡,从而减轻Th2极化.
- 在管理Th2介导的肠道炎症和食物过敏等疾病方面,LR DNA显示出前景.
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