甲暴露会通过激活上皮细胞中的AhR-GDF15通路而加剧喘中的气道重塑
Cuiting Shan1, Wenguan Li1, Yipeng Sun1
1Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Environmental pollution (Barking, Essex : 1987)
|December 19, 2025
概括
酸甲 (BaP) 通过激活酸碳化合物受体 (AhR),增加生长分化因子15 (GDF15),使喘气道重塑恶化. 这种污染物诱导的途径突出显示了喘的潜在治疗标.
科学领域:
- 环境健康 环境健康
- 肺部医学 肺部医学
- 分子生物学分子生物学
背景情况:
- 气道改造,以纤维细胞激活和原沉积为特征,是喘的核心.
- 酸甲 (BaP) 是一种污染物和酸受体 (AhR) 激活剂,与严重的喘有关,但其对呼吸道重塑的影响尚未完全理解.
研究的目的:
- 调查BaP是否通过通过AhR介导的途径增强上皮质-纤维细胞交叉增强气道重塑,从而加剧气道重塑.
- 为了确定参与BaP诱导的气道改造的关键分子媒介.
主要方法:
- 研究了BaP对气道上皮细胞中GDF15表达的影响,评估了AhR与GDF15促进体的结合.
- 评估了BaP治疗细胞中的条件介质对纤维细胞激活 (α-SMA,COL1A1) 和GDF15的作用的影响.
- 在体内评估BaP对过敏原诱导的气道改造的影响,包括原沉积和介质表达.
- 研究了表甲基酸盐 (EGCG) 对AhR和BaP诱导的重塑的影响.
主要成果:
- 在依赖AhR的方式上,BaP上调了表皮GDF15的表达和分泌.
- BaP受条件的介质促进了纤维细胞激活,GDF15敲击减弱了纤维细胞激活.
- 在体内,BaP恶化了过敏原诱导的气道改造,增加了原蛋白,GDF15,α-SMA和COL1A1.1.
- 重组GDF15激活了肺纤维细胞和原蛋白的生产.
- 在体内,EGCG抑制了BaP诱导的GDF15表达和气道重塑.
结论:
- BaP通过由AhR-GDF15轴介导的上皮细胞纤维细胞交叉声加剧了气道重塑.
- 这一途径代表了由环境污染物加剧喘的潜在治疗标.
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