[Establishment of Acinetobacter baumannii-induced pneumonia model in mice].

Objective To establish Acinetobacter baumannii (A. baumannii)-induced pneumonia models in C57BL/6 mice, and study the molecule mechanism of A. baumannii infection. Methods Eighty C57BL/6 mice were divided into normal control group, cyclophosphamide-treated group, A. baumannii infection group, and cyclophosphamide-pretreated A. baumannii infection group. Immunodeficient mice were prepared by injecting cyclophosphamide intraperitoneally. A. baumannii was isolated from intensive care unit (ICU) and fresh bacteria (1×108 CFU/mL) were prepared. Each normal or immunodeficient mouse was inoculated with 50 μL A. baumannii through trachea. The lung, bronchoalveolar lavage fluid (BALF) and blood were collected at 6, 24 and 72 hours after inoculation. The numbers of white blood cells (WBCs) and neutrophils were detected by cell counting. The histopathology of the lung was evaluated by HE staining. Cytokines such as granulocyte macrophage colony-stimulating factor (GM-CSF), interferon γ (IFN-γ), interleukin 1β (IL-1β), IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, tumor necrosis factor α (TNF-α) were detected by ELISA. Results A. baumannii was eliminated within 72 hours after infection in normal mice, whereas the bacteria continued to replicate rapidly in the lungs and blood in the immunodeficient mice. The numbers of WBCs and neutrophils were elevated markedly 6 hours post infection, and return to the normal within 72 hours. However, the numbers of WBCs and neutrophils continuously increased in cyclophosphamide-pretreated A. baumannii infection group, and the pulmonary inflammatory was more severe than that in the normal mice. The cytokines of blood increased markedly 6 hours post infection, and then decreased until 72 hours. However, the cytokines continuously increased in cyclophosphamide-pretreated A. baumannii infection group. Conclusion A. baumannii-induced pneumonia models in C57BL/6 mice were established successfully.