补充维生素D降低交通相关颗粒物暴露的哮喘进展
2018/12/24
背景：最近的文献表明，维生素D缺乏的儿童特别容易受到交通相关空气污染(traffic-related air pollution，TRAP)的影响。因为大部分人口居住在高TRAP暴露区域，所以这项研究意义重大。
目的：我们试图确定补充维生素D能否减轻TRAP暴露对哮喘进展、哮喘急性发作，和（或）气道炎症的影响，并确定补充维生素D获得最大健康获益的最佳时间。
方法学：应用已建立的哮喘小鼠模型，我们检测了产前与产后补充维生素D对哮喘进展的影响，以及在柴油废气颗粒(Diesel exhaust particle，DEP)暴露的环境下，检测维生素D作为已建立哮喘模型的治疗效用。
结果：与对照组相比，DEP和过敏原共同暴露可导致维生素D缺乏小鼠气道高反应性(AHR)增加，并导致致病性TH2/TH17细胞在肺内积聚。产前与产后补充维生素D可显著降低TRAP和过敏原共同暴露后AHR的发展，降低TH2/TH17细胞在肺中的积聚，但不能单独对过敏原作用。一旦哮喘建立，恢复正常的维生素D状态对AHR没有影响。
结论：我们的数据表明，维生素D对哮喘的发生有保护作用，特别是在暴露于TRAP的环境中。虽然补充维生素D并不能逆转既往哮喘，但在DEP激发的过敏性哮喘环境下，早期恢复正常的维生素D状态可明显减弱AHR的发展，并可降低肺TH2/TH17细胞数量，这种细胞可预示重症哮喘的进展情况。
Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.
Bolcas PE, Brandt EB, Zhang Z, Biagini Myers JM, Ruff BP, Khurana Hershey GK.
J Allergy Clin Immunol. 2018 Jun 21. pii: S0091-6749(18)30898-4.
BACKGROUND: 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.
OBJECTIVE: 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.
METHODS: 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.
RESULTS: DEP and allergen coexposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic TH2/TH17 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 TH2/TH17 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.
CONCLUSIONS: 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 TH2/TH17 cells, which portend the development of severe asthma.
目的：我们试图确定补充维生素D能否减轻TRAP暴露对哮喘进展、哮喘急性发作，和（或）气道炎症的影响，并确定补充维生素D获得最大健康获益的最佳时间。
方法学：应用已建立的哮喘小鼠模型，我们检测了产前与产后补充维生素D对哮喘进展的影响，以及在柴油废气颗粒(Diesel exhaust particle，DEP)暴露的环境下，检测维生素D作为已建立哮喘模型的治疗效用。
结果：与对照组相比，DEP和过敏原共同暴露可导致维生素D缺乏小鼠气道高反应性(AHR)增加，并导致致病性TH2/TH17细胞在肺内积聚。产前与产后补充维生素D可显著降低TRAP和过敏原共同暴露后AHR的发展，降低TH2/TH17细胞在肺中的积聚，但不能单独对过敏原作用。一旦哮喘建立，恢复正常的维生素D状态对AHR没有影响。
结论：我们的数据表明，维生素D对哮喘的发生有保护作用，特别是在暴露于TRAP的环境中。虽然补充维生素D并不能逆转既往哮喘，但在DEP激发的过敏性哮喘环境下，早期恢复正常的维生素D状态可明显减弱AHR的发展，并可降低肺TH2/TH17细胞数量，这种细胞可预示重症哮喘的进展情况。
(刘影1 张红萍 1王刚2 四川大学华西医院中西医结合科呼吸病组 610041 摘译)
（J Allergy Clin Immunol. 2018 Jun 21. pii: S0091-6749(18)30898-4.）
（J Allergy Clin Immunol. 2018 Jun 21. pii: S0091-6749(18)30898-4.）
Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure.
Bolcas PE, Brandt EB, Zhang Z, Biagini Myers JM, Ruff BP, Khurana Hershey GK.
J Allergy Clin Immunol. 2018 Jun 21. pii: S0091-6749(18)30898-4.
BACKGROUND: 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.
OBJECTIVE: 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.
METHODS: 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.
RESULTS: DEP and allergen coexposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic TH2/TH17 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 TH2/TH17 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.
CONCLUSIONS: 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 TH2/TH17 cells, which portend the development of severe asthma.
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七氟醚抑制小鼠过敏性气道炎症Th2反应和NLRP3表达
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对哮喘患者口服皮质类固醇激素不良事件和经济影响的一项系统综述
