巨细胞和纤维细胞之间的SPP1介导的交叉声会促进良性气道狭窄
1The First Department of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Respiratory Critical Care Medicine, Hebei Institute of Respiratory Diseases, Shijiazhuang, 050000, Hebei Province, China.
Archives of biochemistry and biophysics
|September 27, 2025
概括
M2巨细胞通过激活纤维细胞信号来驱动气道狭窄纤维化. 用拉巴胺抑制这种途径显示了对良性气道狭窄的治疗潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 肺部病理学 肺部病理学
背景情况:
- 良性气道狭窄涉及复杂的细胞相互作用.
- 了解像巨细胞这样的免疫细胞的作用对于开发有效的治疗方法至关重要.
研究的目的:
- 为了研究M2巨细胞在良性气道狭窄病原发生中的作用.
- 为了探索巨细胞-纤维细胞交叉声的分子机制在呼吸道重塑.
- 为了评估拉帕素作为潜在的治疗剂.
主要方法:
- 使用斯普雷格·道利 (Sprague Dawley) 的呼吸道狭窄的老鼠模型.
- 采用单细胞RNA测序用于对联体受体相互作用的生物信息学分析.
- 在M2巨细胞和纤维细胞的体外共同培养系统中进行.
- 评估了M2巨细胞透和气道重塑标记.
主要成果:
- 增加的M2巨细胞透与呼吸道狭窄的进展相关.
- 通过分泌的蛋白-1 (SPP1) 信号传递,M2巨细胞诱导纤维细胞激活和纤维化.
- 观察到酸丁醇3-酶/蛋白酶B/哺乳动物目标拉巴胺素 (PI3K/AKT/mTOR) 途径的激活.
- 在老鼠中,拉帕米辛治疗减少了颗粒组织,改善了呼吸道通透性.
结论:
- 通过SPP1-介导的PI3K/AKT/mTOR激活在纤维细胞中,M2巨通过SPP1-介导的PI3K/AKT/mTOR激活在良性气道狭窄中促进纤维化气道重塑.
- 用拉帕米辛准SPP1-PI3K/AKT/mTOR轴提供了一个潜在的治疗策略.
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