通过AKT-mTOR通路,TREM2可以改善败血症中的凝血病和肺炎
Chen Zhou1, Chenglong Liang1, Rongrong Zhang2
1The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; Wenzhou Medical University, Wenzhou 325000, China.
International immunopharmacology
|February 19, 2025
概括
在骨髓细胞2 (TREM2) 上表达的触发受体的过度表达改善了生存率,并减少了败血症中的凝血病. TREM2通过抑制巨细胞释放组织因子来减轻炎症.
科学领域:
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
- 分子生物学分子生物学
背景情况:
- 败血症是一种危及生命的感染反应,导致严重的凝血病和炎症.
- 组织因子 (TF) 在败血症中关键地驱动凝血和炎症.
- TREM2在败血症病理生理学中的作用尚不清楚.
研究的目的:
- 研究TREM2在败血症引起的凝血病中的作用.
- 为了确定TREM2是否调节败血症中的巨细胞功能.
- 探索TREM2作为败血症的潜在治疗点.
主要方法:
- 在体外:用脂多糖 (LPS) 刺激的RAW264.7细胞,有或没有TREM2过度表达.
- 在体内:小鼠模型Cecal Ligation and Puncture (CLP) 用TREM2-过度表达的巨细胞.
- 对炎症性细胞因子,凝血因子和信号通路 (AKT-mTOR) 的分析.
主要成果:
- 在小鼠败血症模型中,TREM2过度表达显著提高了生存率.
- TREM2 减少了肺炎,凝血病和纤维素沉积.
- 通过抑制巨细胞中的AKT-mTOR通路,TREM2抑制了TF释放.
结论:
- TREM2对与败血症相关的凝血病有保护作用.
- TREM2代表了改善败血症结果的有希望的治疗标.
- 准TREM2可能为治疗败血症患者提供新的策略.
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