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克拉霉素对铜绿假单胞菌慢性肺部感染小鼠Th1Th2免疫平衡的调节作用
Clarithromycin modulates Th1/Th2 immune balance in mice with chronic Pseudomonas aeruginosa lung infection

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DOI:
作者:
丁凤鸣 朱松雷 沈策 周新
DING fengming, ZHU songlei, SHEN ce, ZHOU xin
作者单位:
上海交通大学附属第一人民医院
Department of respiratory medicine, the first People’s Hospital affiliated to Shanghai Jiao-tong University
关键词:
克拉霉素；铜绿假单胞菌；慢性肺部感染；辅助性T细胞1型；辅助性T细胞2型
Clarithromycin; Pseudomonas aeruginosa; Chronic lung infection; Th1; Th2
摘要:
目的 探讨克拉霉素对铜绿假单胞菌（PA）慢性肺部感染小鼠肺组织Th1/Th2免疫平衡的调节作用。方法 通过小鼠气道接种包裹PA的琼脂糖珠的方法建立PA慢性肺部感染模型。将54只小鼠随机分为克拉霉素治疗组、生理盐水治疗组和对照组。其中克拉霉素治疗组小鼠和生理盐水治疗组小鼠在建模后第7天起分别给予克拉霉素和生理盐水治疗，而对照组小鼠经气道接种无菌琼脂糖珠并接受生理盐水治疗。分别于建模后第7天、第10天和第14天处死小鼠。标本行肺组织细菌培养、病理检查、支气管肺泡灌洗液IFN-γ/IL-4蛋白水平分析和肺组织转录因子T-bet/GATA-3 mRNA水平分析。结果 克拉霉素治疗组小鼠的气道炎症水平得到显著改善。与生理盐水治疗组小鼠相比，克拉霉素治疗组小鼠肺组织的IFN-γ/IL-4比值和T-bet/GATA-3比值分别在接种后第10天和第14天出现显著下调（P < 0.05）。结论 在PA慢性肺部感染初期采用克拉霉素治疗可以使小鼠肺组织的Th1/Th2平衡向Th2偏移，有利于缓解气道炎症。
Objective To investigate the influence of clarithromycin (CAM) treatment on Th1/Th2 immune balance in a mouse model of chronic Pseudomonas aeruginosa (PA) lung infection. Methods We inoculated BALB/c mice with PA-laden agarose beads to establish animal models of chronic PA lung infection. Mice were randomly divided into CAM group, saline group and control group. Mice in CAM group and saline group were inoculated with PA-laden agarose beads, and treated with CAM (CAM group) or saline (saline group) on day 7 after inoculation. Mice in control group were inoculated with sterile beads and treated with saline. Mice were sacrificed on day 7, 10, and 14. The level of bacterial quantification, lung histopathology, Th1/Th2 cytokines and transcription factors were compared among three groups. Results In mice of CAM group, the airway inflammation was significantly relieved, and the ratio of IFN-γ/IL-4 and T-bet/GATA-3 were significantly down-regulated compared with that of saline group on day 10 and day 14, respectively (P < 0.05). Conclusion Our findings suggest that the therapeutic benefits of clarithromycin treatment may be partially due to a shift in the immune systems from Th1 to Th2.

 

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