通过激活ILCs引发的柴油发动机排气引起的非过敏的异氨酸性炎症和气道过敏反应
Huasi Zhao1, Chen Zhan2, Bizhou Li3
1State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Department of Pulmonary and Critial Care Medicine, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, P.R.China; Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R.China.
仅仅暴露于柴油发动机废气 (DEE) 就能在小鼠中引发类似喘的症状,包括气道炎症和过度反应. 天生的淋巴细胞 (ILC) 在这种DEE诱导的反应中起着关键作用.
科学领域:
- 环境健康 环境健康
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 柴油发动机废气 (DEE) 与喘的发展和恶化有关.
- DEE会加剧过敏原引起的肺炎,但其在引发非过敏性炎症方面的作用尚不清楚.
研究的目的:
- 为了调查DEE暴露后的呼吸道炎症和过敏反应.
- 探索DEE暴露与先天性淋巴细胞 (ILC) 之间的关系.
主要方法:
- 小鼠在2,4或6周内暴露在DEE或过空气中.
- 使用特定抗体抑制了先天性淋巴细胞 (ILC) 和CD4+T细胞.
- 评估了气道过敏反应 (AHR),炎症和ILCs.
主要成果:
- 在第4周和第6周,DEE暴露增加了中性粒细胞,性粒细胞和原水平.
- 在DEE暴露4周后,观察到显著的气道过敏反应 (AHR).
- 产生IL-5和IL-17的ILC2和ILC群在DEE暴露时增加,独立于Th2细胞变化.
结论:
- 仅仅暴露于DEE可以在小鼠模型中诱导类似喘的特征.
- 肺内存在的ILCs是DEE诱导的Th2/Th17反应和AHR的关键调解者.
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