S100A8 / A9 在Iatrogenic喉支气管狭窄症中促进纤维化
Laura M Mafla1, Ibrahim Abd-Elazem1, Raymond J So1
1Department of Otolaryngology Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
The Laryngoscope
|August 8, 2025
概括
呼吸道损伤中的关键分子S100A8/A9在阳性喉狭窄症 (iLTS) 中促进纤维化. 针对S100A8/A9和MYD88可能为iLTS提供新的治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
- 病理学 病理学 病理学
背景情况:
- 阳性喉狭窄症 (iLTS) 是由于输管损伤而导致的气道狭窄,而炎症起着关键作用.
- 驱动iLTS病原和纤维化的特定免疫媒介尚未完全理解.
- 单细胞RNA测序显示,iLTS标本中S100A8/A9 (一种与损伤相关的分子模式) 的增加.
研究的目的:
- 在体内调查S100A8/A9在阳性喉狭窄症 (iLTS) 的发展中的作用.
- 确定S100A8/A9是否有助于iLTS中的纤维化过程.
- 在iLTS中探索S100A8/A9的下游信号通路.
主要方法:
- 通过单细胞RNA测序和免疫光在人类iLTS和控制气管组织中评估S100A8/A9表达.
- 在小鼠中诱导iLTS并给药复合S100A8/A9或载体控制以评估纤维性.
- 测量了气管膜自身厚度和与纤维化相关的基因表达 (例如,Col1a1),以量化纤维化.
主要成果:
- 与对照人群相比,人类iLTS组织在自己的膜中显示S100A8 / A9表达的增加.
- 在小鼠中,S100A8/A9治疗显著增加了自己的薄膜厚度 (117.7比67.7μM,p=0.03).
- S100A8/A9治疗导致Col1a1基因表达显著增加 (4.42倍,p=0.01) 和MYD88水平升高.
结论:
- S100A8/A9在人类iLTS中显著存在,并在小鼠模型中驱动纤维化.
- 准S100A8/A9及其下游介质MYD88为iLTS提供了一个潜在的治疗策略.
- 对针对S100A8/A9信号的治疗方法进行进一步的研究是对iLTS治疗的必要.
关键词:
S100A8 / A9 / A9 / S100A8 / A9 / S100A8 / A9 / S100A8 / A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A9 / S100A8 / S100A9 / S100A9 / S100A8 / S100A9 / S100A8 / S100A9 / S100A8 / S100A9 / S100A8 / S100A9 / S100A9 / S100A8 / S100A9 / S100A8 / S100A9 / S100A8 / S100A8 / S100A8 / S100A8 / S100A9纤维化 纤维化喉喉狭窄症 喉狭窄症相关概念视频
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