柴油废气颗粒对大鼠气道反应性及免疫指标影响

Effects of diesel exhaust particles on airway hyperresponsiveness and immunologic index in rats

目的探讨空气污染物中柴油废气课粒(diesel exhaust particle,DEP)吸入对哮喘模型大鼠的气道反应性和免疫学指标的影响。方法选择Wistar大鼠60只,随机分为对照组(A组)、模型组(B组)、实验组(C组、D组、E组、F组),每组各10只。每只大鼠染毒结束后次日处死,并测定每只大鼠气道阻力(RL)30min的变化;采用酶联免疫吸附试验(ELISA)测定血清IgE和肺组织中白介素-5(IL-5)和γ-干扰素(IFN-γ)浓度的变化。结果抗原激发后,B组的气道阻力(7.069±0.632)比A组(3.567±0.211)明显增高;E、F组的气道阻力(8.879±0.616),(11.009±0.693)比B组(7.069±0.632)明显增高(F=156.187,P<0.01);气道阻力增高与DEP吸入时间呈相关性(r=0.948,P<0.01);B组血清中IgE(25.003±1.172)的浓度较A组(20.242±2.143)明显增加(F=2.490,P<0.01);C、E组肺组织中IL-5浓度(17.078±5.235),(18.618±4.228)较B组(12.788±2.827)明显增高(F=4.263,P<0.01);而肺组织中IFN-γ浓度在各组之间比较差异均无统计学意义(F=1.193,P>0.05)。结论柴油废气颗粒吸入可加重哮喘大鼠的气道高反应性,促进血清IgE介导及肺组织中IL-5分泌增加的气道炎症反应。

Objective To investigate the effects of disesel exhaust particles in air pollutants on airway hyperresponsiveness and immunologic index in rats with asthma. Methods Sixty Wistar rats were rendomly divided into 6 groups. Grup A was control group. Group B was animal model group which was ovalbumin （OVA） -sensitized-challenged. Group C,D,E,F were challenged with 3% OVA and then exposed to diesel exhaust particles（DEP） for one to four weeks. The levels of IgE,interleukin-5 （ IL-5 ） and interferon-γ（IFN-γ） of the lung tissue were detected by ELISA. Results The airway hyperresponsiveness of group B increased more than group A. Group B was significantly different from group E and F （ F = 156. 186, P 〈 0.01 ）. Increase of airwag resistance was related with the time of DEP exposure （ r = 0. 948, P 〈 0. 01 ）. The concentration of IgE was significantly different between group A and B（ F = 2. 490 ,P 〈 0. 01 ）. The expression of IL-5 in lung tissue gradually increased in group C. The expression of IL-5 in group B was significantly different from that of group C and E（ F = 4. 263, P 〈 0. 01 ）. The expression of IFN-γ was not significantly different among the groups（ F = 1. 193, P 〉 0. 05 ）. Condusion Exposure to diesel exhaust particles might exacerbate airway hyperresponsiveness and induce airway inflammation caused by IL-5 increase in the rats of asthma model.