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作 者:杜晨[1] 李若瑜[1] 马圣清[1] 王端礼[1]
出 处:《中国麻风皮肤病杂志》2000年第4期216-218,共3页China Journal of Leprosy and Skin Diseases
摘 要: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 detect the variables of gene expression of some cytokines involved in invasive pulmonary aspergillosis (IPA) for deeply research the mechanisms of the disease. Methods:A mice model of IPA was established. The killing activities of pulmonary macrophages against spores of Aspergillus fumigagatus was compared in vitro by determining the colony forming unit per milliter (CFU/ml), and the level of cytokines in the lung tissue was examined by RT PCR. Results:In model group, the killing activities of pulmonary macrophages were significantly lowered. Upon infection, the mice in model group had lower gene espression of IFN γ with continually higher that of IL 10. Conclusion :The down regulated activities of pulmonary macrophages and the dysfunction of Th1/Th2 cytokines may play an important role in the pathogenesis of IPA. [
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