Ambient ultrafine particles provide a strong adjuvant effect in the secondary immune response: implication for traffic-related asthma flares
Ambient ultrafine particles provide a strong adjuvant effect in the secondary immune response: implication for traffic-related asthma flares
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DOI：
10.1152/ajplung.00115.2010
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发表时间：
2010-09-01
影响因子：
4.9
通讯作者：
Nel, Andre E.
中科院分区：
文献类型：
--
作者：
Li, Ning;Harkema, Jack R.;Nel, Andre E.
首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容周围的超细颗粒在二次免疫反应中提供了强大的佐剂作用：这意味着与交通相关的哮喘发作。Am J Physiol肺细胞分子Physiol 299：L374-L383,2010。2010年6月18日首次出版；DOI：10.1152/ajpeng.00115.2010。-我们之前已经证明，鼻腔给药环境超细颗粒(UFP)可作为BALB/c小鼠对卵清蛋白(OVA)的初级过敏增敏的佐剂。重要的是要找出吸入UFP对二次免疫反应的影响是否与解释已经过敏的人因高速公路附近的交通暴露而出现哮喘发作的方式相同。这项研究的目的是确定吸入城市高速公路附近环境中的UFP是否可以增强已经致敏的小鼠对OVA的二次免疫反应。在我们位于洛杉矶的流动动物实验室中，先前的OVA致敏动物在第二次OVA挑战时暴露于浓缩的环境UFP中。评估OVA特异性抗体产生、气道形态计量学、过敏性气道炎症、细胞因子基因表达和氧化应激标志物。与鼻内滴注UFP对初级免疫反应的佐剂作用相比，只需五次环境中的UFP暴露就足以促进OVA Recall免疫反应，包括在较小和更远的呼吸道产生过敏性呼吸道炎症。二次免疫反应以T辅助细胞因子2和IL-17细胞因子基因在肺内的表达为特征。综上所述，我们的结果表明，吸入氧化前环境中的UFP可以有效地增强对实验变应原的二次免疫反应，这表明车辆交通暴露可能会加剧已经致敏的受试者的过敏性炎症。
Li N, Harkema JR, Lewandowski RP, Wang M, Bramble LA, Gookin GR, Ning Z, Kleinman MT, Sioutas C, Nel AE. Ambient ultrafine particles provide a strong adjuvant effect in the secondary immune response: implication for traffic-related asthma flares. Am J Physiol Lung Cell Mol Physiol 299: L374-L383, 2010. First published June 18, 2010; doi:10.1152/ajplung.00115.2010.-We have previously demonstrated that intranasal administration of ambient ultrafine particles (UFP) acts as an adjuvant for primary allergic sensitization to ovalbumin (OVA) in Balb/c mice. It is important to find out whether inhaled UFP exert the same effect on the secondary immune response as a way of explaining asthma flares in already-sensitized individuals due to traffic exposure near a freeway. The objective of this study is to determine whether inhalation exposure to ambient UFP near an urban freeway could enhance the secondary immune response to OVA in already-sensitized mice. Prior OVA-sensitized animals were exposed to concentrated ambient UFP at the time of secondary OVA challenge in our mobile animal laboratory in Los Angeles. OVA-specific antibody production, airway morphometry, allergic airway inflammation, cytokine gene expression, and oxidative stress marker were assessed. As few as five ambient UFP exposures were sufficient to promote the OVA recall immune response, including generating allergic airway inflammation in smaller and more distal airways compared with the adjuvant effect of intranasally instilled UFP on the primary immune response. The secondary immune response was characterized by the T helper 2 and IL-17 cytokine gene expression in the lung. In summary, our results demonstrated that inhalation of prooxidative ambient UFP could effectively boost the secondary immune response to an experimental allergen, indicating that vehicular traffic exposure could exacerbate allergic inflammation in already-sensitized subjects.