中文摘要：

目的免疫抑制小鼠经气管切开注入烟曲霉孢子悬液建立侵袭性肺曲霉病（IPA）动物模型并动态观察其肺组织病理改变，以期为IPA研究提供在体模型及观察IPA疾病发展过程。方法C57BL／6J小鼠经腹腔注射250mg／kg环磷酰胺×2次构建免疫抑制状态；麻醉状态下于小鼠颈部切开-0．3cm小口，分离出气管并接种烟曲霉临床株；动态观察小鼠一般情况、生存率、肺部真菌负荷、肺组织大体及病理变化。结果小鼠感染烟曲霉后第4天死亡率为100％；感染后第1天肺部曲霉孢子含量最高，后逐渐降低；肺组织大体表现为出血、水肿及白色菌团结节，呈逐渐加重趋势；病理发现肺泡内炎症细胞渗出，以淋巴细胞浸润为主，肺组织大量出血、坏死，随时间延长而加重，最终正常肺泡结构消失。结论通过环磷酰胺腹腔注射使小鼠免疫抑制，经气管切开成功建立了IPA小鼠模型，过度炎症反应是其死亡的重要原因。

英文摘要：

Objective Immunosuppressed mice were injected with suspension of Aspergillus fumigates spore by tracheotomy to establish invasive pulmonary aspergillosis （IPA） animal models and pathological changes of lung tissue were dynamically observed in order to provide a basis for the IPA mouse studies and learn more about IPA disease development. Methods C57BL/6J mice were intraperitoneally injected with cyelophosphamide 250 mg/kg twice, building immune suppression. Under anesthesia,the neck of mice was cut a 0.3 cm incision, the trachea was isolated and inoculated with Aspergillus fumigatus. The mice general state, survival, pulmonary fungal load, gross and pathological changes in lung tissue were dynamically observed. Results The mortality rate on the fourth day after Aspergillus fumigatus infection in mice was 100%. The content of Aspergillus spores in lungs on the first day was the highest, and then decreased. The gross observation showed lung tissue bleeding, edema, and white fungus loci,and the degree gradually increased. Pathological results showed alveolar inflammatory cells,including lymphocytes infiltration, heavy bleeding and necrosis increased with time, the normal alveolar structure gradually disappeared. Conclusions By intraperitoneal injection of cyclophosphamide, mice are immunosuppressed, and mouse model of Aspergillus infection is successfully established by tracheotomy,excessive inflammatory response is an important reason of death.