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增强的CHI3L1在性间歇性囊炎的持续性炎症事件中促进巨细胞激活
Wei Zhang1, Yize Guo1, Jiawen Wang2
1Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Frontiers in immunology
|February 16, 2026
概括
CHI3L1蛋白通过改变巨细胞的新陈代谢和促进糖解,驱动汉纳型间歇性囊炎/膀疼痛综合征 (HIC/BPS) 的慢性炎症. 这表明CHI3L1是HIC/BPS的关键治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢途径 代谢途径
- 慢性炎症是一种慢性炎症.
背景情况:
- 间歇性囊炎/膀疼痛综合征 (IC/BPS),特别是汉纳型IC/BPS (HIC),涉及慢性炎症和巨细胞功能障碍.
- CHI3L1在HIC上升调节,与疾病严重程度有关,但其在巨介导炎症中的作用尚不清楚.
研究的目的:
- 研究CHI3L1在巨驱动炎症和HIC中的代谢变化中的作用.
- 确定CHI3L1的信号通路和作为治疗点的潜力.
主要方法:
- 集成的IC/BPS患者数据的多omics分析.
- 利用循环胺诱导的小鼠模型进行体内验证.
- 在CHI3L1-过度表达的巨细胞进行了体外功能测定.
主要成果:
- 在HIC患者中,CHI3L1的调节升高,与炎症标志物相关.
- 在巨细胞中CHI3L1过度表达促进了前炎性通路 (NF-κB,TNF) 和糖解.
- CHI3L1抑制了线粒体的氧化酸化和酸盐代谢,与MYC信号相关.
结论:
- CHI3L1通过重编程巨细胞代谢,使其转向糖解,从而加剧HIC中的持续性炎症事件.
- CHI3L1通过MYC信号维持炎症,使其成为HIC中的中央调节者.
- 通过破坏免疫代谢循环,CHI3L1代表了HIC的潜在治疗标.
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