Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production
Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production
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DOI：
10.1016/j.jaci.2006.04.050
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发表时间：
2006-08-01
影响因子：
14.2
通讯作者：
Tsicopoulos, Anne
中科院分区：
文献类型：
--
作者：
Chang, Ying;Senechal, Stephanie;Tsicopoulos, Anne
背景资料：过敏性疾病的患病率在过去20年中有所增加，许多研究表明，柴油机尾气颗粒相关的多环芳烃会加剧过敏反应。关于它们在非特应性受试者中产生T（H）2型过敏反应的潜在能力知之甚少。目的：本研究的目的是检验柴油机废气暴露可能有利于非特应性供体T（H）2型细胞募集的假设，无论是通过增加T（H）2吸引趋化因子的产生还是减少T（H）1吸引趋化因子的产生。将来自非特应性供体的PBMC与柴油机尾气颗粒-多环芳烃一起孵育，并评估上清液中pro-T（H）1趋化因子的存在（IFN-γ诱导蛋白10和IFN-γ诱导的单核因子）和pro-T（H）2趋化因子（巨噬细胞衍生的趋化因子，I-309，以及肺和活化调节的趋化因子）。结果：柴油机尾气暴露于非特应性供体PBMC 48 h后，肺组织IL-13介导的活化调节趋化因子水平增加，IFN-γ诱导的蛋白10水平选择性降低，但差异无统计学意义（P> 0.05）。这些趋化因子变异的功能效应导致T（H）2细胞趋化性增强，而T（H）1细胞则无此作用。结论：柴油机尾气暴露可能通过差异调节趋化因子促进非特应性受试者T（H）2细胞的募集而参与过敏性疾病的发生。环境因素，特别是空气污染，可能有利于过敏性疾病的发生。
Background: The prevalence of allergic diseases has increased in the last 20 years, and a number of studies have shown that diesel exhaust particle-associated polyaromatic hydrocarbons can exacerbate the allergic reaction. Much less is known about their potential capacity to generate a T(H)2-type allergic reaction in nonatopic subjects.Objective: The aim of this study was to test the hypothesis that diesel exhaust exposure might favor, in nonatopic donors, T(H)2-type cell recruitment, either through increased production of T(H)2-attracting chemokines or decreased production of T(H)1-attracting chemokines.Methods: PBMCs from nonatopic donors were incubated with diesel exhaust particle-polyaromatic hydrocarbons, and the supernatants were evaluated for the presence of pro-T(H)1 chemokines (IFN-gamma-induced protein 10 and monokine Induced by IFN-gamma) and pro-T(H)2 chemokines (macrophage-derived chemokine, I-309, and pulmonary and activation-regulated chemokine) by means of ELISA. The functional effect was evaluated by using chemotaxis assays with polarized T(H)1 and T(H)2 cells.Results: Diesel exhaust exposure of PBMCs from nonatopic donors induced a late increase after 48 hours in pulmonary and activation-regulated chemokine mediated by IL-13 and a decrease in IFN-gamma-induced protein 10 levels selectively at both the protein and mRNA levels. The functional effect of these chemokine variations resulted in an enhanced chermotaxis of T(H)2, but not T(H)1, Cells.Conclusion: These findings show that diesel exhaust exposure might be involved in the genesis of allergic diseases by differentially regulating chemokines favoring the recruitment of T(H)2 cells in nonatopic subjects.Clinical implications: Environmental factors, especially air pollution, might favor the genesis of allergic diseases.