铜绿假单胞菌肺部感染对小鼠 Toll 样受体 2、4 的影响

目的探讨Toll样受体（TLR）2、4mRNA在铜绿假单胞菌慢性感染小鼠肺内的动态改变及其作用。方法56只雄性Balb／c小鼠随机气道接种含有铜绿假单胞菌（PA）琼脂糖珠（感染组，34只）和无菌琼脂糖珠（对照组，22只）。于第1、3、5、7、10天处死小鼠，取肺组织细菌培养，行肺组织病理观察，ELISA法检测肺泡灌洗液（BALF）中自介素（IL）-6和IL-17的含量，采用Real—timePCR检测TLR2mRNA及TLR4mRNA表达。结果感染组在接种后第3天IL-6和IL-17水平均达高峰，分别为（154．83±12．51）ng／L和（601．05±25．53）ng／L，均显著高于对照组（40．05±2．98）ng／L和（213．75±9．25）ng／L，差异有统计学意义（P〈0．05），且两者在接种后第10天仍处于高水平。感染组中TLR4mRNA的相对表达量第7天达高峰（4．09±0．25），与对照组第7天（0．97±0．05）比较，差异有统计学意义（P〈0．05）；而TLR2mRNA在感染组和对照组各时间相比变化均不明显（P〉0．05）。结论TLR4与小鼠肺部慢性感染PA的发生发展密切相关，其机制可能与TLR4在肺的免疫损伤中起到重要作用有关。

The changes of TLR2 and TLR4 on chronic Pseudomonas aeruginosa lung infection in mice

Objective To investigate the function changes of toll like receptor （TLR） 2, 4 in mice with chronic Pseu- domonas aeruginosa （PA） lung infection. Methods 56 male Balb/c mice were randomly given the airway inoculated with PA agarose beads （infection group, n=34） and sterile agarose beads （control group, n=22）. On day 1, 3, 5, 7, 10 after infection, mice were sacrificed. Lung tissue bacterial cultures and lung pathology were observed, interleukin （IL）-6 and IL-17 in bronchoalveolar lavage fluid （BALF） were observed by ELISA. The mRNA expression of TLR2 and TLR4 were detected by Real-time PCR. Results Compared with control group, IL-6, IL-17 levels were up to the highest levels of infection group on day 3, data of infection group were （154.83±12.51） ng/L and （601.05±25.53） ng/L, significantly higher than control group, which were （40.05±2.98） ng/L and （213.75±9.25） ng/L, the differences were statistically significant （P 〈 0.05）; and both of them were still at high levels on day 10. On day 7 the mRNA expression of TLR4 reached a peak of （4.09±0.25） in the infection group, and the control group was （0.97±0.05）, the difference was statistically signif- icant （P 〈 0.05）, while no significant changes of TLR2 existed in the two groups in each time （P 〉 0.05）. Conclusion TLR4 is closely related to the occurrence and development on chronic Pseudomonas aeruginosa lung infection in mice, and the mechanism is that TLR4 may he crucial for its development of immune and inflammatory injury.