Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Immunology Graduate Program, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio.
Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
J Allergy Clin Immunol. 2019 Jan;143(1):386-394.e3. doi: 10.1016/j.jaci.2018.04.042. Epub 2018 Jun 21.
Recent literature suggests that children who are vitamin D deficient are uniquely susceptible to the effects of traffic-related air pollution (TRAP) exposure. This is highly significant because large segments of the population reside in zones of high TRAP exposure.
We sought to determine whether vitamin D supplementation mitigates the effect of TRAP exposure on asthma development, asthma exacerbation, and/or airway inflammation and to determine the timing of vitamin D supplementation that confers maximal health benefit.
Using established mouse models of asthma, we examined the effect of prenatal and postnatal vitamin D supplementation on asthma development, as well as the utility of vitamin D as a treatment for established asthma in the context of diesel exhaust particle (DEP) exposure.
DEP and allergen coexposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic T2/T17 cells in the lungs of vitamin D-deficient mice compared with control mice. Prenatal and postnatal vitamin D supplementation significantly attenuated the development of AHR and decreased pulmonary accumulation of T2/T17 cells after coexposure to TRAP and allergen but not to allergen alone. Restoration of normal vitamin D status had no effect on AHR once asthma was already established.
Our data establish that vitamin D confers protection against asthma development specifically in the context of TRAP exposure. Although vitamin D replacement did not reverse established asthma, restoration of normal vitamin D status in early life significantly attenuated the development of AHR in the setting of DEP-exacerbated allergic asthma and reduced numbers of lung T2/T17 cells, which portend the development of severe asthma.
最近的文献表明，维生素 D 缺乏的儿童对交通相关空气污染（TRAP）暴露的影响特别敏感。这一点非常重要，因为很大一部分人口居住在 TRAP 暴露水平高的地区。
我们试图确定维生素 D 补充是否能减轻 TRAP 暴露对哮喘发展、哮喘恶化和/或气道炎症的影响，并确定维生素 D 补充的最佳时间，以获得最大的健康益处。
我们使用已建立的哮喘小鼠模型，研究了产前和产后维生素 D 补充对哮喘发展的影响，以及在柴油 exhaust particle (DEP) 暴露的情况下，维生素 D 作为治疗已建立的哮喘的效用。
DEP 和过敏原共同暴露导致维生素 D 缺乏的小鼠气道高反应性（AHR）增加和致病性 T2/T17 细胞在肺部的积累，与对照小鼠相比。与对照小鼠相比，产前和产后维生素 D 补充显著减弱了 AHR 的发展，并减少了 TRAP 和过敏原共同暴露后 T2/T17 细胞在肺部的积累，但对过敏原单独暴露没有影响。一旦哮喘已经建立，恢复正常的维生素 D 状态对 AHR 没有影响。
我们的数据表明，维生素 D 特异性地在 TRAP 暴露的情况下提供对哮喘发展的保护。虽然维生素 D 替代不能逆转已建立的哮喘，但在 DEP 加重过敏性哮喘的情况下，早期恢复正常的维生素 D 状态显著减弱了 AHR 的发展，并减少了肺部 T2/T17 细胞的数量，这预示着严重哮喘的发展。
