Kepley Christopher L, Lauer Fredine T, Oliver Janet M, Burchiel Scott W
Department of Internal Medicine, Medical College of Virginia, 1112 East Clay Street, McGuire Hall, Richmond, VA 23298, USA.
Clin Immunol. 2003 Apr;107(1):10-9. doi: 10.1016/s1521-6616(03)00004-4.
Polycyclic aromatic hydrocarbons (PAHs) are major components of diesel exhaust particles found in pollutant respirable particles. There is growing evidence that these fossil fuel combustion products exacerbate allergic inflammation. Basophils contribute to allergic inflammation through the release of preformed and granule-derived mediators. To determine whether allergens and PAHs interact, we incubated human basophils with PAHs and measured the release of histamine and IL-4 with and without added antigen. None of the PAHs induced mediator release by itself and none affected total cellular histamine levels. However, several PAHs enhanced histamine release and IL-4 production in response to crosslinking the high-affinity IgE receptor, Fc epsilon RI. The enhancement seen with 1,6-BaP-quinone involved an increase in tyrosine phosphorylation in several different substrates, including the Fc epsilon RI-associated tyrosine kinase, Lyn, and elevated reactive oxygen species (ROS) levels detected by dichlorofluorescein fluorescence and flow cytometry. The PAH-induced enhancement of mediator release and ROS production could be inhibited with the antioxidant N-acetylcysteine. These data provide further evidence that environmental pollutants can influence allergic inflammation through enhanced Fc epsilon RI-coupled mediator release from human basophils.
多环芳烃（PAHs）是可吸入污染物颗粒中柴油尾气颗粒的主要成分。越来越多的证据表明，这些化石燃料燃烧产物会加剧过敏性炎症。嗜碱性粒细胞通过释放预先形成的和颗粒衍生的介质来促进过敏性炎症。为了确定过敏原和多环芳烃是否相互作用，我们将人嗜碱性粒细胞与多环芳烃一起孵育，并在添加和不添加抗原的情况下测量组胺和白细胞介素-4的释放。没有一种多环芳烃能单独诱导介质释放，也没有一种会影响细胞内组胺的总水平。然而，几种多环芳烃在高亲和力IgE受体FcεRI交联后增强了组胺释放和白细胞介素-4的产生。1,6-苯并芘醌所观察到的增强作用涉及几种不同底物中酪氨酸磷酸化的增加，包括与FcεRI相关的酪氨酸激酶Lyn，以及通过二氯荧光素荧光和流式细胞术检测到的活性氧（ROS）水平升高。多环芳烃诱导的介质释放和ROS产生的增强可被抗氧化剂N-乙酰半胱氨酸抑制。这些数据进一步证明，环境污染物可通过增强人嗜碱性粒细胞中FcεRI偶联的介质释放来影响过敏性炎症。
