饮酒会通过激活PI3K/AKT/mTOR通路介导的Th1分化来加剧实验性自身免疫性前列腺炎
Shun Xu1,2,3, Jing Chen1,2,3, Shaoyu Yue1,2,3
1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, China.
Frontiers in immunology
|January 28, 2025
概括
酒精消费通过PI3K/AKT/mTOR通路促进Th1细胞分化,使慢性前列腺炎/慢性骨盆疼痛综合征 (CP/CPPS) 恶化. 这一途径为CP/CPPS提供了潜在的治疗点.
科学领域:
- 泌尿器科 泌尿器科 泌尿器科 泌尿器科
- 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:
- 流行病学研究将酒精消费与慢性前列腺炎/慢性骨盆疼痛综合征 (CP/CPPS) 联系起来.
- 酒精对CP/CPPS的影响背后的机制尚不清楚.
- 本研究使用动物模型和人类数据调查酒精对CP/CPPS的影响.
研究的目的:
- 确定酒精消费如何影响CP/CPPS.
- 阐明涉及酒精诱导的CP/CPPS恶化的分子机制.
- 为了确定CP/CPPS的潜在治疗点.
主要方法:
- 建立了实验性自身免疫性前列腺炎 (EAP) 鼠标模型.
- 在EAP诱导和评估炎症期间服用酒精.
- 利用蛋白质组分析,流动细胞计和西式涂抹来研究机制.
- 包括患有慢性酒精消费的患者,以获得临床相关性.
主要成果:
- 酒精消费加剧了小鼠和患者的EAP严重程度.
- 发现了异常的Th1分化和PI3K/AKT/mTOR通路激活.
- 酒精激活了PI3K/AKT/mTOR通路,增加了Th1细胞的分化.
- 抑制PI3K (LY294002) 降低了Th1分化,并缓解了EAP炎症.
结论:
- 酒精摄入促进Th1细胞分化,并通过激活PI3K/AKT/mTOR通路而加剧EAP.
- PI3K/AKT/mTOR通路是CP/CPPS中酒精有害作用的关键调解者.
- 抑制PI3K/AKT/mTOR通路为CP/CPPS提供了一个潜在的治疗策略.
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