Matsumoto Aki, Hiramatsu Kumiko, Li Yingji, Azuma Arata, Kudoh Shoji, Takizawa Hajime, Sugawara Isamu
Fourth Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
Clin Immunol. 2006 Nov;121(2):227-35. doi: 10.1016/j.clim.2006.08.003. Epub 2006 Sep 18.
In conjunction with allergens, diesel exhaust particles act as an adjuvant to enhance IgE responses, inducing expression of cytokines/chemokines and adhesion molecules, and increasing airway hyper-responsiveness (AHR). As most studies were designed to expose animals to diesel exhaust throughout the periods of both sensitization and allergen challenge, it remains unclear whether diesel exhaust (DE) exposure exaggerates airway responses in asthmatic animals.
To study effects of exposure to low-dose DE on AHR and allergic airway inflammation in asthmatic mice.
BALB/c mice were sensitized by intraperitoneal injection of ovalbumin and challenged by intranasal administration with ovalbumin. They were exposed to low-dose DE for 7 h/day, 5 days/week, for up to 12 weeks. AHR to methacholine was evaluated by whole-body plethysmography as well as bronchoalveolar lavage cell analysis and cytokine gene expression in lungs.
Repeated exposure of asthmatic mice to low-dose DE resulted in increased AHR and gene expression of several pro-asthmatic cytokines/chemokines, but these effects rapidly subsided with continued exposure to DE.
Repeated exposure to low-dose DE after ovalbumin challenge exaggerates allergic responses in mice, but effects are not prolonged with continuous DE exposure.
柴油废气颗粒与过敏原共同作用，作为佐剂增强IgE反应，诱导细胞因子/趋化因子和黏附分子的表达，并增加气道高反应性（AHR）。由于大多数研究设计为在致敏和过敏原激发两个阶段都让动物暴露于柴油废气中，柴油废气（DE）暴露是否会加剧哮喘动物的气道反应仍不清楚。
研究低剂量DE暴露对哮喘小鼠AHR和过敏性气道炎症的影响。
通过腹腔注射卵清蛋白使BALB/c小鼠致敏，并用卵清蛋白经鼻给药进行激发。它们每天暴露于低剂量DE 7小时，每周5天，持续长达12周。通过全身体积描记法以及支气管肺泡灌洗细胞分析和肺中细胞因子基因表达来评估对乙酰甲胆碱的AHR。
哮喘小鼠反复暴露于低剂量DE导致AHR增加以及几种促哮喘细胞因子/趋化因子的基因表达增加，但随着持续暴露于DE，这些作用迅速消退。
卵清蛋白激发后反复暴露于低剂量DE会加剧小鼠的过敏反应，但持续暴露于DE不会延长这些作用。
