Fernvik E, Peltre G, Sénéchal H, Vargaftig B B
Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur-INSERM U485, Paris, France.
Clin Exp Allergy. 2002 Apr;32(4):602-11. doi: 10.1046/j.0954-7894.2002.01347.x.
Health effects due to air pollution arising from motor vehicles are a major public and political concern world-wide. Epidemiological studies have shown that the manifestations of asthma are increased by air pollution in already affected individuals.
To investigate the potential role of air-polluted tunnel dust (traffic particulate matter, TPM) or pure carbon core particles in the initiation and persistence of experimental allergic inflammation.
BP2 mice were immunized with birch pollen alone (group B) or pollen together with TPM (group A), or with birch pollen and Al(OH)3 (group C), or with birch pollen and carbon core particles (group D). Before methacholine challenge they were challenged intranasally and thereafter bronchial hyper-reactivity (BHR) was evaluated in a whole-body plethysmograph. Levels of Th2 cytokines, fibronectin and lactate dehydrogenase (LDH) were determined, and differential counts were performed in the bronchoalveolar lavage (BAL) fluid. Sera were collected for determination of antibody titres and cytokine levels.
Specific IgE titres, BHR, the number of recruited eosinophils and levels of fibronectin and LDH in BAL were increased in mice immunized and challenged with a mixture of birch pollen and TPM. However, mice immunized with birch pollen alone and challenged intranasally with pollen or a mixture of pollen and TPM demonstrated the highest levels of IL-4 and IL-5.
This study highlights the importance of the exposure to a combination of particulate matters and pollen allergens, in the induction of allergic disease in the airways, and we have demonstrated that polluted tunnel dust has an effect on both the inflammatory and immunological components of experimental allergy. Immunization and challenge with carbon core particles together with birch pollen increased neither the BHR nor the specific IgE production significantly. Our results therefore strongly suggest that it is most likely to be the organic phase bound to the carbon core of the diesel exhaust particles that might have an important adjuvant effect in the induction of experimental allergy.
机动车造成的空气污染对健康的影响是全球主要的公共和政治关注点。流行病学研究表明，空气污染会使已受影响个体的哮喘症状加重。
研究空气污染的隧道灰尘（交通颗粒物，TPM）或纯碳核颗粒在实验性变应性炎症的引发和持续中的潜在作用。
用桦树花粉单独免疫BP2小鼠（B组），或用花粉与TPM一起免疫（A组），或用桦树花粉和氢氧化铝免疫（C组），或用桦树花粉和碳核颗粒免疫（D组）。在乙酰甲胆碱激发前，对它们进行鼻内激发，然后在全身体积描记仪中评估支气管高反应性（BHR）。测定Th2细胞因子、纤连蛋白和乳酸脱氢酶（LDH）水平，并对支气管肺泡灌洗（BAL）液进行细胞分类计数。收集血清以测定抗体滴度和细胞因子水平。
用桦树花粉和TPM混合物免疫并激发的小鼠，其特异性IgE滴度、BHR、募集的嗜酸性粒细胞数量以及BAL中纤连蛋白和LDH水平均升高。然而，单独用桦树花粉免疫并经鼻用花粉或花粉与TPM混合物激发的小鼠，其IL-4和IL-5水平最高。
本研究强调了暴露于颗粒物和花粉过敏原组合在气道变应性疾病诱导中的重要性，并且我们已经证明污染的隧道灰尘对实验性变应性炎症的炎症和免疫成分均有影响。用碳核颗粒与桦树花粉一起免疫和激发，既未显著增加BHR，也未显著增加特异性IgE的产生。因此，我们的结果强烈表明，很可能是与柴油废气颗粒碳核结合的有机相在实验性变应性炎症的诱导中可能具有重要的佐剂作用。
