Kurup V P, Guo J, Murali P S, Choi H, Fink J N
Department of Medicine, Medical College of Wisconsin, Veterans Affairs Medical Center, Milwaukee 53295, USA.
J Lab Clin Med. 1997 Dec;130(6):567-75. doi: 10.1016/s0022-2143(97)90106-2.
Two strains of interleukin-4 (IL-4) gene knockout mice were studied and compared with wild strains to determine the role of IL-4 in the immunopathogenesis of murine allergic aspergillosis. Animals immunized intraperitoneally were subsequently challenged with Aspergillus antigen intranasally. The animals were evaluated for total serum immunoglobulin E (IgE) levels, Aspergillus-specific IgG antibody isotypes, peripheral blood eosinophils, cytokine and chemokine mRNA transcripts in spleen cells, and pulmonary histology. No serum IgE was detected in animals deficient in the IL-4 gene. Aspergillus-specific IgG1 was detected in all animals, while enhanced levels of IgG2a were detected in IL-4 knockout animals challenged with A. fumigatus antigen. There were no differences in the peripheral blood or lung eosinophils in the two groups of mice exposed to A. fumigatus. These results indicate that lung injury in Aspergillus-antigen challenged animals may be the result of the eosinophil mediators and that IgE-mediated injury may not be significant in this model, which may be a significant variation between the model and human allergic aspergillosis.
研究了两株白细胞介素-4（IL-4）基因敲除小鼠，并与野生株进行比较，以确定IL-4在小鼠过敏性曲霉病免疫发病机制中的作用。腹腔内免疫的动物随后经鼻用曲霉抗原进行攻击。对动物进行了总血清免疫球蛋白E（IgE）水平、曲霉特异性IgG抗体亚型、外周血嗜酸性粒细胞、脾细胞中的细胞因子和趋化因子mRNA转录本以及肺组织学评估。在IL-4基因缺陷的动物中未检测到血清IgE。在所有动物中均检测到曲霉特异性IgG1，而在用烟曲霉抗原攻击的IL-4基因敲除动物中检测到IgG2a水平升高。在暴露于烟曲霉的两组小鼠中，外周血或肺嗜酸性粒细胞没有差异。这些结果表明，曲霉抗原攻击动物的肺损伤可能是嗜酸性粒细胞介质的结果，并且在该模型中IgE介导的损伤可能不显著，这可能是该模型与人类过敏性曲霉病之间的显著差异。
