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目的建立小鼠侵袭性肺曲霉菌病(IPA)的动物模型。方法将90只小鼠随机分为5组,模型组:于接种前4天和接种前1天腹腔注射环磷酰胺200 mg/kg,通过鼻腔吸入浓度为1×1011/L烟曲霉菌孢子悬液40μl。非环磷酰胺对照组:除以0.9%氯化钠注射液(NS)代替环磷酰胺外,其余操作同模型组。环磷酰胺对照组:以NS代替烟曲霉菌滴鼻,其余操作同模型组。空白对照组:用NS代替环磷酰胺行腹腔注射,以NS代替烟曲霉菌孢子,其余操作同模型组。重组人粒细胞集落刺激因子(G-CSF)组:在模型组基础上,接种真菌孢子1天后皮下注射G-CSF 20μg kg-1 d-1。通过肺组织病理、肺组织真菌培养和血清半乳甘露聚糖测定(GM试验)等确定肺侵袭性曲霉菌病模型是否构建成功。结果肺曲霉菌培养、血清GM试验和病理切片等结果均表明,模型组和G-CSF组均发生了IPA,其余各组均无IPA发生。结论成功建立了小鼠肺曲霉菌模型。
Objective To establish an animal model of mouse aggressive pulmonary aspergillosis (IPA). Methods Ninety mice were randomly divided into five groups. In the model group, cyclophosphamide (200 mg / kg) was injected intraperitoneally 4 days before vaccination and 1 day before inoculation. The mice were inoculated intranasally with a concentration of 1 × 10 11 / L of Aspergillus fumigatus spores suspension Liquid 40μl. Non-cyclophosphamide control group: except for 0.9% sodium chloride injection (NS) instead of cyclophosphamide, the rest of the operation with the model group. Cyclophosphamide control group: NS substituting Aspergillus fumigatus intranasal, the rest of the operation with the model group. Blank control group: NS instead of cyclophosphamide were injected intraperitoneally with NS instead of Aspergillus fumigatus spores, the rest of the operation with the model group. Recombinant human granulocyte-colony stimulating factor (G-CSF) group: On the basis of the model group, G-CSF 20 μg kg-1 d-1 was injected subcutaneously 1 day after inoculation of fungal spores. Lung invasiveness of aspergillosis models were successfully established through lung histopathology, lung tissue fungal culture and serum galactomannan assay (GM test). Results Aspergillus influenzae culture, serum GM test and pathological results showed that IPA occurred in both model group and G-CSF group, and no IPA occurred in other groups. Conclusion The mouse model of pulmonary aspergillus was successfully established.