Kurup V P, Choi H Y, Murali P S, Xia J Q, Coffman R L, Fink J N
Department of Medicine, Medical College of Wisconsin, VA Medical Center, Milwaukee 53295, USA.
Allergy. 1999 May;54(5):420-7. doi: 10.1034/j.1398-9995.1999.00944.x.
Exposure to Aspergillus fumigatus allergens results in enhanced total serum IgE and peripheral blood eosinophils in mice. The associated pulmonary inflammation and immunologic responses are comparable to those detected in human allergic bronchopulmonary aspergillosis. Allergen-induced cytokines are thought to regulate the inflammatory and immune responses in these animals.
In the present study, we exposed C57BL/6 and BALB/c mice to A. fumigatus antigen. Both wild-type and IL-4 knockout phenotypes of animals of both strains were used. Some animals were also treated with anti-IL-5 or anti-IFN-gamma. Total serum IgE, Aspergillus species IgG subclass, peripheral blood eosinophils, and lung histology were studied.
The results demonstrate similar lung inflammation in all wild-type and IL-4-/- animals exposed to A. fumigatus antigen. Similarly, in spite of the diverse immune response produced by the anticytokine treatment, no major differences were detected among any of the animal groups studied.
It can be concluded that A. fumigatus exposure in an immunologically unaltered host is predominantly of a Th2 type, and that depletion of the Th2 cytokine leads to a similar lung inflammation but with a characteristic Th1 response, suggesting that the pathogenesis of allergic aspergillosis is the result of multiple induction pathways.
暴露于烟曲霉变应原会导致小鼠血清总IgE和外周血嗜酸性粒细胞增加。相关的肺部炎症和免疫反应与人类过敏性支气管肺曲霉病中检测到的情况相当。变应原诱导的细胞因子被认为可调节这些动物的炎症和免疫反应。
在本研究中，我们将C57BL/6和BALB/c小鼠暴露于烟曲霉抗原。使用了两种品系动物的野生型和IL-4基因敲除表型。一些动物还用抗IL-5或抗IFN-γ进行了处理。研究了血清总IgE、曲霉属IgG亚类、外周血嗜酸性粒细胞和肺组织学。
结果表明，所有暴露于烟曲霉抗原的野生型和IL-4基因敲除动物都有相似的肺部炎症。同样，尽管抗细胞因子治疗产生了不同的免疫反应，但在所研究的任何动物组之间均未检测到重大差异。
可以得出结论，在免疫未改变的宿主中暴露于烟曲霉主要是Th2型，Th2细胞因子的耗竭会导致类似的肺部炎症，但具有特征性的Th1反应，这表明过敏性曲霉病的发病机制是多种诱导途径的结果。
