Chu H W, Wang J M, Boutet M, Laviolette M
Unité de Recherche, Hôpital Laval, Université Laval, Ste-Foy, Québec, Canada.
Lab Anim Sci. 1996 Feb;46(1):42-7.
Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) are two important proinflammatory cytokines that may be involved in allergic inflammatory processes. We recently developed a murine model of allergic bronchopulmonary aspergillosis characterized by eosinophilic and lymphocyte lung infiltration and increased serum and bronchoalveolar lavage immunoglobulin E concentration. In this study we examined the expression of TNF-alpha and IL-1 alpha in the lung tissue sections of C57BL/6 mice that were intranasally challenged with Aspergillus fumigatus antigen or saline on the first 3 days of each week and sacrificed on days 4, 7, 14, and 21. Compared with the control mice, A. fumigatus treated mice had a remarkable increase of TNF-alpha and IL-1 alpha expression in the lung on days 4, 14, and 21, with a slight increase on day 7. The major types of cells expressing TNF-alpha and IL-1 alpha included alveolar macrophages, endothelial cells, and bronchiolar and alveolar epithelial cells. Consistent with increased expression of TNF-alpha and IL-1 alpha, intercellular adhesion molecule-1 expression also was upregulated in the lung of A. fumigatus treated mice; its time course and cell types were similar to those of TNF-alpha and IL-1 alpha expression. These results suggest that TNF-alpha and IL-1 alpha may be involved in the A. fumigatus induced inflammatory process and that upregulated intercellular adhesion molecule-1 expression may represent one of the roles played by TNF-alpha and IL-1 alpha in this murine model.
肿瘤坏死因子-α(TNF-α)和白细胞介素-1α(IL-1α)是两种重要的促炎细胞因子,可能参与过敏性炎症过程。我们最近建立了一种过敏性支气管肺曲霉病的小鼠模型,其特征为嗜酸性粒细胞和淋巴细胞浸润肺组织以及血清和支气管肺泡灌洗免疫球蛋白E浓度升高。在本研究中,我们检测了C57BL/6小鼠肺组织切片中TNF-α和IL-1α的表达,这些小鼠每周的前3天经鼻用烟曲霉抗原或生理盐水攻击,并在第4、7、14和21天处死。与对照小鼠相比,烟曲霉处理的小鼠在第4、14和21天肺中TNF-α和IL-1α的表达显著增加,在第7天略有增加。表达TNF-α和IL-1α的主要细胞类型包括肺泡巨噬细胞、内皮细胞以及细支气管和肺泡上皮细胞。与TNF-α和IL-1α表达增加一致,烟曲霉处理的小鼠肺中细胞间黏附分子-1的表达也上调;其时间进程和细胞类型与TNF-α和IL-1α表达相似。这些结果表明,TNF-α和IL-1α可能参与了烟曲霉诱导的炎症过程,并且细胞间黏附分子-1表达上调可能代表了TNF-α和IL-1α在该小鼠模型中所起的作用之一。