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来自木烟和道路交通的颗粒物的过敏佐剂效应。

Allergy adjuvant effect of particles from wood smoke and road traffic.

作者信息

Samuelsen Mari, Nygaard Unni Cecilie, Løvik Martinus

机构信息

Division of Environmental Medicine, Norwegian Institute of Public Health, P.O.Box 4404 Nydalen, NO-0403 Oslo, Norway.

出版信息

Toxicology. 2008 Apr 18;246(2-3):124-31. doi: 10.1016/j.tox.2008.01.001. Epub 2008 Jan 15.

DOI:10.1016/j.tox.2008.01.001
PMID:18289765
Abstract

There is growing evidence that in addition to augmenting the severity of asthma and allergic diseases, particulate air pollution also increases the incidence of allergy and asthma. We studied the adjuvant effect of particles from wood smoke and road traffic on the immune response to the allergen ovalbumin (OVA). OVA with and without particles was injected into one hind footpad of Balb/cA mice. All particles together with OVA significantly increased the level of OVA-specific immunoglobulin E (IgE) in serum, compared to groups given OVA or particles alone. Reference diesel exhaust particles (DEP) with OVA induced the highest levels of IgE, whereas no clear difference was observed between particles from road traffic and wood smoke. Road traffic particles collected in the autumn induced higher IgE values with OVA than corresponding particles collected during the winter season when studded tires are used, suggesting that studded tire-generated road pavement particles have less allergy adjuvant activity than exhaust particles. Compared to OVA or particles alone, all particles with OVA increased popliteal lymph node cell numbers, cell proliferation, ex vivo secretion of IL-4 and IL-10 after ConA stimulation, and the expression of several cell surface molecules (CD19, MHC class II, CD86 and CD23). Wood smoke particles with OVA induced somewhat higher cellular responses than road traffic particles, but less than DEP with OVA which seemed to be the most potent particle in inducing cellular as well as antibody responses. Thus, wood smoke particles had about the same capacity to enhance allergic sensitization as road traffic particles, but less than diesel exhaust particles.

摘要

越来越多的证据表明,除了加剧哮喘和过敏性疾病的严重程度外,颗粒物空气污染还会增加过敏和哮喘的发病率。我们研究了木烟和道路交通产生的颗粒物对过敏原卵清蛋白(OVA)免疫反应的佐剂作用。将含有和不含有颗粒物的OVA注射到Balb/cA小鼠的一只后足垫中。与单独给予OVA或颗粒物的组相比,所有颗粒物与OVA一起显著提高了血清中OVA特异性免疫球蛋白E(IgE)的水平。参考柴油尾气颗粒(DEP)与OVA诱导产生的IgE水平最高,而道路交通和木烟产生的颗粒物之间未观察到明显差异。秋季收集的道路交通颗粒物与OVA一起诱导产生的IgE值高于使用防滑轮胎的冬季收集的相应颗粒物,这表明防滑轮胎产生的路面颗粒物的过敏佐剂活性低于尾气颗粒。与单独给予OVA或颗粒物相比,所有颗粒物与OVA一起增加了腘窝淋巴结细胞数量、细胞增殖、ConA刺激后IL-4和IL-10的体外分泌,以及几种细胞表面分子(CD19、MHC II类、CD86和CD23)的表达。木烟颗粒与OVA诱导的细胞反应略高于道路交通颗粒,但低于DEP与OVA,DEP似乎是诱导细胞和抗体反应最有效的颗粒。因此,木烟颗粒增强过敏致敏的能力与道路交通颗粒大致相同,但低于柴油尾气颗粒。

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