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目的 : 观察侵袭性肺曲霉病 (invasivepulmonaryaspergillosis,IPA)发病过程中相关细胞因子基因表达的变化 ,进一步探讨其发病机制。方法 : 建立小鼠IPA模型 ,采用平板菌落计数法比较正常组与模型组肺巨噬细胞在体外对烟曲霉孢子的杀伤活性 ;采用RT PCR检测肺组织细胞因子 (cytokine ,CK)的产生情况。结果 : 在模型组中 ,巨噬细胞对孢子的杀伤活性明显降低 ;感染后 ,模型组IFN γ产生较正常组明显降低 ,而IL 10在感染第 1天及第 5天均维持高水平。结论 : 肺巨噬细胞功能降低、Th1 Th2型CK调节失衡在IPA发病中起重要作用。
OBJECTIVE: To observe the changes of gene expression related cytokines during the pathogenesis of invasive pulmonary aspergillosis (IPA) and to explore its pathogenesis. Methods: The mouse IPA model was established. The colony counts of lung were used to compare the cytotoxic activity of lung macrophages in vitro to Aspergillus fumigatus spores. The level of cytokine (CK) in lung tissue was detected by RT-PCR. Results: In the model group, the killing activity of macrophages to spores was significantly reduced. After infection, the IFNγ production in the model group was significantly lower than that in the normal group, while the level of IL-10 remained high on the first day and the fifth day after infection. Conclusions: The function of pulmonary macrophages is decreased. The imbalance of Th1-type and Th2-type CK plays an important role in the pathogenesis of IPA.