红霉素对烟草烟雾暴露肺气肿小鼠肺组织树突状细胞33D1及共刺激分子CD40、CD80、CD86表达的影响

Effects of Erythromycin on Expression of Pulmonary Dendritic Cell33D1 and Costimulatory Molecules CD40,CD80 and CD86 in Tobacco Smoke-exposed Mice with Emphysema

目的:观察红霉素对烟草烟雾暴露肺气肿模型小鼠肺组织树突状细胞33D1及共刺激分子CD40、CD80、CD86表达的影响,为临床防治提供依据。方法:SPF级balb/c小鼠随机分为四个组,空白对照组,模型组,红霉素预防组和红霉素治疗组,每组各10只,模型组和红霉素治疗组给予烟熏24周建立小鼠肺气肿模型,红霉素预防组从第20周开始给予红霉素(80 mg/kg)灌胃预防治疗共4周;红霉素治疗组从第25周开始给予红霉素(80 mg/kg)灌胃预防治疗共4周,然后处死各组小鼠,取出小鼠外周血,肺泡灌洗液,肺组织,常规HE染色观察各组小鼠肺部病理改变,免疫组化检测肺组织中树突状细胞33D1的表达情况,PCR检测共刺激分子CD40、CD80、CD86mRNA的浓度。结果:常规病理观察烟草烟雾暴露24周小鼠肺组织均出现典型肺气肿改变,红霉素干预后肺部炎性反应减轻;免疫组化结果:与对照组和红霉素预防组比较,模型组气道和肺组织中树突状细胞33D1阳性细胞数均明显增多,红霉素治疗后33D1阳性细胞数下降,但仍高于模型对照组,差异有统计学意义(P<0.05);PCR结果:与对照组相比,模型组肺组织中共刺激分子CD40、CD80、CD86mRNA明显增多,红霉素干预后下降,但仍高于对照组,差异有统计学意义(P<0.05)。结论:树突状细胞及共刺激分子参与肺气肿发病,红霉素可下调肺气肿肺组织树突状细胞及共刺激分子表达水平,减轻肺气肿肺部炎性反应,具体机制有待进一步研究。

Objective To observe the effects of erythromycin on the expression of pulmonary dendritic cell 33D1 and costimulatory molecules CD40,CD80 and CD86 in tobacco smoke-exposed mice with emphysema,providing a basis for clinical prevention and treatment.Method SPF balb/c mice were randomly divided into blank control group,model group,erythromycin prevention group and erythromycin treatment group,10 mice in each group.In model group and erythromycin treatment group,a pulmonary emphysema model was established in mice by exposing to tobacco smoke for 24 weeks.The erythromycin prevention group was intragastrically administered with erythromycin(80 mg/kg)for 4 weeks from the 20 th week.The erythromycin treatment group was intragastrically administered with erythromycin(80 mg/kg)for 4 weeks from the 25 th week.Subsequently,all the mice were killed and their peripheral blood,broncho-alveolar lavage fluid and lung tissues were collected.Pathological changes in the lung were observed by routine HE staining.The expression of pulmonary dendritic cell 33D1 was detected using immunohistochemistry.The mRNA expressions of costimulatory molecules CD40,CD80 and CD86 were detected by PCR.Results Typical emphysema changes showed typical emphysema changes in the lung tissue of mice exposed to tobacco smoke for 24 weeks.Pulmonary inflammation was alleviated after erythromycin intervention.Immunohistochemical results demonstrated that compared with the control group and the erythromycin prevention group,the number of 33D1-positive dendritic cells in the airway and lung tissue of the model group increased significantly,and decreased after erythromycin treatment,but still higher than that of the model control group(P<0.05).PCR results revealed that compared with the control group,the mRNA expression of costimulatory molecules CD40,CD80 and CD86 in the lung of the model group increased significantly,and decreased after erythromycin intervention,but still higher than that of the control group(P<0.05).Conclusion Dendritic cells and costimulatory molecules participate in the pathogenesis of emphysema.Erythromycin can down-regulate the expression of dendritic cell and costimulatory molecules in the lung and alleviate pulmonary inflammation in emphysema.However,the specific mechanism needs further study.