Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.

Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.
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维生素 D 补充剂可减轻交通相关颗粒物暴露后的哮喘发展。

DOI:
10.1016/j.jaci.2018.04.042
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发表时间:
2019-01
期刊:
The Journal of allergy and clinical immunology
影响因子:
--
通讯作者:
Khurana Hershey GK
Khurana Hershey GK
中科院分区:
其他
文献类型:
--
作者:
Bolcas PE;Brandt EB;Zhang Z;Biagini Myers JM;Ruff BP;Khurana Hershey GK

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最近的文献表明,缺乏维生素D的儿童特别容易受到与交通有关的空气污染(TRAP)的影响。这是非常重要的,因为大部分人口居住在TRAP高暴露区。确定补充维生素D是否能减轻TRAP暴露对哮喘发展、哮喘加重和/或气道炎症的影响,并确定补充维生素D的时机,以获得最大的健康益处。利用已建立的哮喘小鼠模型,我们研究了产前和产后补充维生素D对哮喘发展的影响,以及维生素D作为柴油废气颗粒(DEP)暴露背景下已建立的哮喘治疗的效用。与对照组小鼠相比,DEP和过敏原共同暴露导致维生素D缺乏小鼠气道高反应性(AHR)和肺部致病性Th2/Th17细胞的积累增加。产前和产后补充维生素D可显著减弱AHR的发展,并减少TRAP和过敏原共同暴露后肺中Th2/Th17细胞的积累,但不能单独暴露于过敏原。一旦哮喘已经建立,恢复正常的维生素D水平对AHR没有影响。我们的数据表明,维生素D对哮喘的发展具有保护作用,特别是在TRAP暴露的情况下。虽然维生素D替代并不能逆转已建立的哮喘,但在生命早期恢复正常的维生素D状态可显著减轻急性加重的过敏性哮喘中AHR的发展,并减少肺Th2/Th17细胞,这预示着严重哮喘的发展。
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. To determine whether vitamin D supplementation mitigates the impact 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 impact of pre-and post-natal 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 co-exposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic Th2/Th17 cells in the lungs of vitamin D deficient mice compared to control mice. Prenatal and postnatal vitamin D supplementation significantly attenuated the development of AHR, and decreased pulmonary accumulation of Th2/Th17 cells following co-exposure to TRAP and allergen, but not allergen alone. Restoration of normal vitamin D status had no impact 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. While vitamin D replacement did not reverse established asthma, restoration of normal vitamin D status in early life significantly attenuated the development of AHR in DEP-exacerbated allergic asthma and reduced lung Th2/Th17 cells, which portend the development of severe asthma.
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