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维生素 D(3) 缺乏可增强变应原诱导的过敏性气道疾病小鼠模型中的淋巴细胞反应。

Vitamin D(3) deficiency enhances allergen-induced lymphocyte responses in a mouse model of allergic airway disease.

机构信息

Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia.

出版信息

Pediatr Allergy Immunol. 2012 Feb;23(1):83-7. doi: 10.1111/j.1399-3038.2011.01146.x.

DOI:10.1111/j.1399-3038.2011.01146.x
PMID:22283404
Abstract

There is debate as to whether vitamin D deficiency contributes towards the extent of the asthma epidemic. In this study, using a mouse model, we determined whether vitamin D deficiency in utero and during early life modulated the severity of asthma. Using dietary restriction, vitamin D(3) -replete and vitamin D(3) -deficient colonies of BALB/c mice were established. Utilizing the allergic airway disease model of asthma with the experimental allergen ovalbumin (OVA), we examined asthma-like responses 24 h after airway challenge with OVA in adult offspring born to vitamin D(3) -replete and vitamin D(3) -deficient mothers. The ability of airway-draining lymph node cells to proliferate and secrete cytokines in response to OVA ex vivo was significantly enhanced by vitamin D(3) deficiency. However, other aspects of allergic disease, including the numbers and proportions of inflammatory cells and cytokines in the lungs and the quantity of OVA-specific IgE in serum, were not modified. These results suggest that vitamin D(3) deficiency modulates the capacity of lymphocytes to respond to allergens.

摘要

关于维生素 D 缺乏是否会导致哮喘流行的严重程度,目前存在争议。在这项研究中,我们使用小鼠模型,确定宫内和生命早期的维生素 D 缺乏是否会调节哮喘的严重程度。通过饮食限制,建立了 BALB/c 小鼠的维生素 D(3)充足和维生素 D(3)缺乏的菌落。利用过敏性气道疾病哮喘模型和实验过敏原卵清蛋白 (OVA),我们检测了出生于维生素 D(3)充足和维生素 D(3)缺乏母亲的成年后代在 OVA 气道挑战后 24 小时的哮喘样反应。气道引流淋巴结细胞对 OVA 的体外增殖和细胞因子分泌能力因维生素 D(3)缺乏而显著增强。然而,过敏疾病的其他方面,包括肺部炎症细胞和细胞因子的数量和比例以及血清中 OVA 特异性 IgE 的量,并没有改变。这些结果表明,维生素 D(3)缺乏会调节淋巴细胞对过敏原的反应能力。

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