通过IL-13受体α1表达作用的香烟烟雾提取物诱导的杯状细胞转化和激增的增强
Akina Mori1, Risa Matsumoto1, Sakuya Ichikawa1
1Scientific Product Assessment Center, Japan Tobacco Inc., 6-2, Umegaoka, Aoba-Ku, Yokohama, Japan.
Toxicology letters
|June 18, 2025
概括
香烟烟雾提取物和IL-13协同增加气道细胞中的粘液产生. 香烟烟雾会激活基碳化合物受体,增强IL-13受体的表达,并促进杯状细胞的转化和增生.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 慢性呼吸道炎症,在COPD中见到,导致杯状细胞转化和增生 (GCMH),导致粘液过度产生和空气流量限制.
- 香烟烟雾是慢性呼吸道炎症和GCMH的主要原因,涉及复杂的机制和免疫细胞.
- 以前的研究表明,香烟烟雾对上皮细胞有直接影响.
研究的目的:
- 为了研究香烟烟雾提取物 (CSE) 和中白素-13 (IL-13) 对正常人支气管上皮细胞 (NHBE) 中的GCMH的协同作用.
- 阐明CSE诱导GCMH的信号通路,重点关注IL-13受体表达和酸受体 (AhR) 激活.
主要方法:
- 来自单个非吸烟者的培养NHBE在空气液体接口处暴露于CSE和/或IL-13.
- 在CSE暴露后测量IL-13受体表达,特别是IL-13Rα1.
- 亚利碳化合物受体 (AhR) 的作用使用酸和AhR抑制剂复星进行了评估.
主要成果:
- 与单次暴露相比,与IL-13和CSE同时暴露会协同增强粘液的产生.
- 暴露于CSE显著增加了IL-13受体亚单元IL-13Rα1.1的表达.
- 甲 (一种AhR配体) 以剂量依赖的方式增加了IL-13Rα1的表达,而白醇 (一种AhR抑制剂) 阻断了CSE的影响.
结论:
- 香烟烟雾通过AhR刺激上调IL-13Rα1的表达,从而使上皮细胞对IL-13敏感,从而诱导GCMH.
- 这项研究揭示了一种新的途径,有助于慢性呼吸道炎症和GCMH.
- 这些发现支持了体外模型的实用性,用于研究慢性炎症而不需要共同培养免疫细胞.
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