Components of diesel exhaust particles differentially affect Th1/Th2 response in a murine model of allergic airway inflammation
Components of diesel exhaust particles differentially affect Th1/Th2 response in a murine model of allergic airway inflammation
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DOI：
10.1111/j.1365-2222.2006.02452.x
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发表时间：
2006-03-01
影响因子：
6.1
通讯作者：
Hayakawa, K
中科院分区：
文献类型：
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作者：
Yanagisawa, R;Takano, H;Hayakawa, K
背景柴油机尾气颗粒物(DEP)可加重多种呼吸系统疾病。然而，目前尚不清楚DEP中的哪些成分与增强有关。采用DEP残存碳核(洗涤DEP)、DEP中有机化合物(OC)提取(DEP-OC)、DEP-OC+洗涤DEP(完整DEP)和卵白蛋白(OVA)对抗原相关气道炎症的影响。结果DEP-OC比洗涤后的DEP更能促进BAL液中炎性细胞的浸润、炎症程度的加重和气道上皮杯状细胞的增殖，与OVA存在时肺组织嗜酸性粒细胞和IL-5的表达增强以及OVA特异性IgG1的浓度升高相平行。相比之下，洗涤DEP加OVA组变化较小，并增加了肺组织中干扰素-γ的表达。整体DEP和OVA的联合应用引起了最显著的变化，同时伴随着IL-13和巨噬细胞炎性蛋白-1α表达的增强。结论DEP-OC而不是洗涤的DEP通过增强T辅助细胞的2型反应而加重了过敏性气道炎症。OC与碳核共存引起的加重最为显著。DEP组分可能对各种呼吸系统疾病有不同程度的影响，而整体DEP可能主要加重呼吸系统疾病。
Background Diesel exhaust particles (DEP) can enhance various respiratory diseases. However, it is unclear as to which components in DEP are associated with the enhancement. We investigated the effects of DEP components on antigen-related airway inflammation, using residual carbonaceous nuclei of DEP after extraction (washed DEP), extracted organic chemicals (OC) in DEP (DEP-OC), and DEP-OC plus washed DEP (whole DEP) in the presence or absence of ovalbumin (OVA).Methods Male ICR mice were intratracheally administrated with OVA and/or DEP components. We examined the cellular profile of bronchoalveolar lavage (BAL) fluid, histological changes, lung expression of inflammatory molecules, and antigen-specific production of IgG1 in the serum.Results DEP-OC, rather than washed DEP, enhanced infiltration of inflammatory cells into BAL fluid, magnitude of airway inflammation, and proliferation of goblet cells in the airway epithelium in the presence of OVA, which was paralleled by the enhanced lung expression of eotaxin and IL-5 as well as the elevated concentration of OVA-specific IgG1. In contrast, washed DEP with OVA showed less change and increased the lung expression of IFN-gamma. The combination of whole DEP and OVA caused the most remarkable changes in the entire enhancement, which was also accompanied by the enhanced expression of IL-13 and macrophage inflammatory protein-1 alpha.Conclusion DEP-OC, rather than washed DEP, exaggerated allergic airway inflammation through the enhancement of T-helper type 2 responses. The coexistence of OC with carbonaceous nuclei caused the most remarkable aggravation. DEP components might diversely affect various types of respiratory diseases, while whole DEP might mostly aggravate respiratory diseases.