Murine strain differences in airway inflammation induced by diesel exhaust and house dust mite allergen

已知屋尘螨与当今哮喘患病率的增加有关。将三种小鼠（BALB/c、ICR和C3 H/He）暴露于烟尘浓度为3.0 mg/m^3的DE或纯空气中8周。这些小鼠在8周的暴露期间以2周的间隔用1 μ g Der f气管内注射4次。研究了小鼠气道的组织学变化、肺中哮喘相关细胞因子和趋化因子以及血浆中变应原特异性免疫球蛋白。DE暴露引起所有品系小鼠气道中的非纤毛细胞增殖和上皮细胞肥大，并且在C3 H/He小鼠的支气管上皮中显示非常轻微的杯状细胞增殖和气道中嗜酸性粒细胞募集。derf处理后，三株小鼠气道内嗜酸性粒细胞增多，杯状细胞增生。其递增顺序为BALB/c < ICR <C3 H/He小鼠。DE+Der f组与Der f组相比，能显著增加BALB/c小鼠和ICR小鼠嗜酸性粒细胞的募集，并增加ICR小鼠杯状细胞的增殖。然而，这些病理变化减少的情况下，C3 H/He小鼠。DE+Der f可使IL-5、eotaxin和RANTES水平增加，MCP-1和MIP-1 α水平协同增加。DE+Der f组小鼠肺组织中IL-5、eotaxin及血浆中Der f特异性IgG 1含量的增加顺序为BALB/c < ICR <C3 H/He小鼠。肺组织中IL-5的产生水平与DE和/或Der f治疗引起的嗜酸性气道炎症的表现相对应。DE暴露的加重作用可能主要通过增加局部IL-5、eotaxin的表达来介导。抗原特异性IgG 1可能是过敏性哮喘发病机制中的重要免疫球蛋白，并可能增强DE。

House dust mites have known to implicate the increase of asthma prevalence today. Three strains of mice (BALB/c, ICR, and C3H/He) were exposed to DE at-a soot concentration of 3.O mg/m^3 or cline air for 8 weeks. These mice injected intratracheally with 1 μ g of Der f four times at 2-week intervals during 8 weeks of the exposure. Histopathological changes in the murine airway, asthma relevant cytokines and chemokines in the lungs, and allergen-specific immunoglobulins in plasma were investigated. DE exposure caused non-ciliated cell proliferation and epithelial cell hypertrophy in the airway of the all strains, and showed very slight goblet cell proliferation in the bronchial epithelium and eosinophil recruitment in the airway of the C3H/He mice. Der f treatment exhibited the recruitment of eosinophils and proliferation of goblet cells in the airway of the three strains. The increasing order of magnitude of those was BALB/c < ICR < C3H/He mice. DE+Der f increased significantly the recruitment of eosinophils in the BALB/c and ICR mice, and increased goblet cell proliferation in the ICR mice compared with Der f treatment. However, these phathologic changes decreased in the case of the C3H/He mice. DE+Der f caused the additional increases of IL-5, eotaxin and RANTES, and synergistic increases of MCP-1 and MIP-1 a in the three strains. The increasing order of IL-5 and eotaxin in lung tissues and Der f-specific lgG1 in plasma by DE+Der f was BALB/c < ICR < C3H/He mice. The production levels of IL-5 in lung tissues corresponded to the manifestations of eosinophilic airway inflammation by DE and/or Der f treatment. The aggravating effect of DE exposure may be mediated mainly by the increase of local expression of IL-5, eotaxin. Antigen-specific lgG1 suggests to be an important immunoglobulin in the pathogenesis of allergic asthma and in the enhancement of DE.