大鼠铜绿假单胞菌肺炎模型的评价及其炎性因子的变化

目的 建立耐药铜绿假单胞菌感染致肺炎的大鼠模型,对模型大鼠肺病理学、细菌学及血清炎性指标变化进行评价。方法 采用经口气管插管法建立耐药铜绿假单胞菌感染致肺炎大鼠模型,造模后观察大鼠一般状态、记录体质量变化,并分别在感染后24、48、72、120 h检查肺组织病理学变化和肺组织活菌菌落计数;应用抗体芯片技术探析耐药铜绿假单胞菌感染后大鼠血清炎性因子的动态变化规律,寻找差异性炎性因子。结果 大鼠感染耐药铜绿假单胞菌后,出现精神状态差、寒颤、呼吸频数高等肺炎的典型表现;感染后各时间点体质量均明显低于对照组,差异有统计学意义（P<0.05）;肺组织病理切片呈典型肺炎表现,肺组织匀浆细菌培养后有典型铜绿假单胞菌菌落生长,以上均达到了肺炎模型建立标准。耐药铜绿假单胞菌感染后大鼠血清中9种炎性因子水平发生明显变化,其中IL-1β、IL-6、TNF-α、IFN-γ、IL-10、ICAM-1及MCP-1水平在感染后显著升高,差异有统计学意义（P<0.05）;TIMP-1水平在感染早期有降低的趋势,感染后期则明显升高,差异有统计学意义（P<0.05）;L-selectin水平在感染后呈先升高后下降的变化,差异有统计学意义（P<0.05）。结论 本研究成功建立了耐药铜绿假单胞菌感染致肺炎的大鼠模型,感染后大鼠炎症免疫反应失调,可为进一步探究铜绿假单胞感染的耐药机制提供参考依据。

Rat model of pneumonia induced by Pseudomonas aeruginosa and the change of inflammatory cytokine

Objective To establish a rat model of pneumonia induced by drug-resistant Pseudomonas aeruginosa infection, and evaluate the changes in lung pathology, bacteriology and serum inflammatory indexes of the infected rats. Methods The rat model of pneumonia induced by drug-resistant Pseudomonas aeruginosa infection was established by oral tracheal intubation. After modeling, the general state of the rat was observed and the weight change was recorded. The pathological changes of lung tissue and the count of viable bacterial colonies in lung tissue were examined at 24, 48, 72 , 120 h. Antibody chip technology was used to analyze the dynamic changes of serum inflammatory cytokines of the infected rats, and the differential inflammatory cytokines were sought. Results After being infected by drug-resistant Pseudomonas aeruginosa, the rats appeared typical symptoms of pneumonia such as poor mental state, chills, and high respiratory rate. The body weights of infected rats at different time points were significantly decreased (vs control group, P<0.05). The pathological section of lung tissues of infected rats showed typical pneumonia, and typical Pseudomonas aeruginosa colonies appeared on the medium after culturing lung tissue homogenate. All of the above had reached the standards of establishing a pneumonia model. In addition, the levels of 9 inflammatory cytokines of the infected rats changed significantly. Among them, the levels of IL-1β, IL-6, TNF-α, IFN-γ, IL-10, ICAM-1 and MCP-1 increased significantly after infection (vs control group, P<0.05); TIMP-1 level showed a downward trend in the early stage of infection, and increased significantly in the later stage of infection (vs control group, P<0.05); L-selectin level increased first and then decreased after infection (vs control group, P<0.05). Conclusion This study successfully established a rat model of pneumonia induced by drug-resistant Pseudomonas aeruginosa infection, accompanied by a disorder of inflammatory immune response, which provides a basis for further exploring the drug resistance mechanism of Pseudomonas aeruginosa infection.