大鼠慢性绿脓杆菌生物膜肺部感染模型细胞因子水平的变化

目的:探讨人工绿脓杆菌(PA)生物膜肺部感染大鼠模型肺部细胞因子水平的变化.方法:由支气管内直接注入PA(菌种为PA0579)藻酸盐微粒(1×109CFU/mL),建立慢性PA生物膜肺部感染大鼠模型,以支气管内注入生理盐水作为对照,两周后评估各组动物肺部IL-4、IFN-γ及TNF-α水平及肺组织病理学的变化.结果:PA感染两周后,PA感染组的肺部炎症反应严重,其急性炎症(PMN≥90%,MN≤10%)的发生率明显高于慢性炎症(MN≥90%,PMN≤10%)发生率(P<0.05),镜下观察在PA藻酸盐微菌珠周围有大量的PMN浸润,而假模型组及正常组的肺部组织切片未见异常.肺部细胞因子检测发现.PA感染组肺部IL-4水平及TNF-α水平均显著高于假模型组和正常组(P<0.01,P<0.001),肺部IFN-γ水平却明显低于后两组(P<0.01).结论:PA生物膜肺部感染可能通过诱导Th2型免疫反应为主,从而引发以多形核向细胞浸润为主的Ⅲ型变态反应所导致的肺组织损害.

Cytokine changes of biofilm in a rat model of chronic pseudomonas aeruginosa pulmonary infection

Objective ：To observe the cytokine modulating effect of biofilm in a rat model of chronic pseudomonas aeruginosa pulmonary infection. Methods： Rats were challenged intratracheally with alginate embedded PA strain PAO579 in the concentration of 1×10^9 colony-forming units per milliliter （CFU/ML）and saline was used as a placebo. Two weeks later intratracheal challenge with P. aerugi- nosa, parameters was evaluated. Results ：Two weeks after challenge,a significant infiltration of numerous polymorphonuclear leukocytes （PMN） in the lung tissues with higher IL-4.TNF-α and lower IFN-γ production in the lungs were found in the PA-infected group compared to the placebo group and nomal control group （P〈0.01 ,P〈0.001）. Meanwhile,the incidence of chronic inflammatio （MN ≥90%, PMN ≤10% ） was significantly lower than acute inflammation （PMN ≥ 90%, MN ≤ 10%） in the PA-infected group（P〈0.05）. Conclusion： PA biofilm can induce Th2 like immune responses （antibody-mediated immunity） which might lead to lung tissues damage of m type hypersensitivith with infiltrating numerous PMN.