IL-33/ST2轴介导柴油废气颗粒诱导的大细胞激活
Wun-Hao Cheng1,2, Ting-Li Zhuang1,2, Meng-Jung Lee3
1School of Respiratory Therapy, Taipei Medical University College of Medicine, 250 Wu-Hsing Street, Taipei, 11031, Taiwan.
Molecular medicine (Cambridge, Mass.)
|December 20, 2024
概括
空气中的污染物,如柴油废气颗粒,通过基碳化合物受体 (AhR) 和NF-κB通路激活细胞 (MC). 这会触发IL-33和2型细胞因子的释放,使喘恶化.
科学领域:
- 免疫学 免疫学 免疫学
- 环境健康 环境健康
- 呼吸系统医学 呼吸系统医学
背景情况:
- 乳腺细胞 (MC) 是喘病变的关键参与者,通过介质释放驱动2型 (T2) 炎症.
- 激活的巨细胞在儿童和成年人群中对喘的严重程度有显著的贡献.
研究的目的:
- 调查柴油废气颗粒 (DEP) 在巨细胞激活和介质蛋白-33 (IL-33) 生产中的作用.
- 阐明信号通路,包括参与DEP诱导的瘤细胞反应的烯碳化合物受体 (AhR).
- 了解DEP介导的杆细胞激活如何影响2型细胞因子的释放和气道迁移.
主要方法:
- 从暴露于DEP的Balb/c小鼠的气道组织中分析了巨细胞透和IL-33表达.
- 人类巨细胞 (HMC-1) 在体外用DEP进行刺激,以评估IL-33和细胞因子的产生.
- 使用siRNA和特定抑制剂检查了AhR,ARNT和NF-κB通路的参与.
主要成果:
- 在小鼠中DEP灌注增加了IL-33表达性杆细胞在气道组织中的透.
- 在人类巨细胞中,DEP暴露通过AhR/ARNT通路调节了IL-33和2型细胞因子 (IL-4,IL-5,IL-13) 的产生.
- DEP激活了NF-κB,促进了AhR的核转移,增强了乳腺细胞迁移,其作用被抗ST2抗体阻断.
结论:
- 像DEP这样的空气中的污染物可以通过AhR/NF-κB通路激活乳腺细胞.
- 这种激活导致IL-33和2型细胞因子的产生增加.
- IL-33/ST2轴促进巨细胞向气道上皮层迁移,可能加剧喘.
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