Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.
Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.
复制标题
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:
影响因子:
--
通讯作者:
Khurana Hershey GK
中科院分区:
文献类型:
--
作者:
Bolcas PE;Brandt EB;Zhang Z;Biagini Myers JM;Ruff BP;Khurana Hershey GK
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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影响因子:
14.2
作者:
Manners, Sarah;Alam, Rafeul;Schwartz, David A.;Gorska, Magdalena M.
通讯作者:
Gorska, Magdalena M.
影响因子:
8.6
作者:
Fawaz, Lama;Mrad, May F.;Khoury, Samia J.
通讯作者:
Khoury, Samia J.
影响因子:
2.2
作者:
Litonjua AA;Lange NE;Carey VJ;Brown S;Laranjo N;Harshfield BJ;O'Connor GT;Sandel M;Strunk RC;Bacharier LB;Zeiger RS;Schatz M;Hollis BW;Weiss ST
通讯作者:
Weiss ST
影响因子:
3.1
作者:
Bar Yoseph, Ronen;Livnat, Galit;Bentur, Lea
通讯作者:
Bentur, Lea
影响因子:
14.2
作者:
Alessandrini, F;Schulz, H;Jakob, T
通讯作者:
Jakob, T