CD1a^(+)和CD83^(+)树突状细胞在COPD小鼠肺组织中的分布及意义  

Distribution and significance of CD1a^(+)and CD83^(+)dendritic cells in lung tissue of COPD mice

作　　者：张兰英 张福安 刘茂茂 陈杰 周健 刘钰婷 欧阳瑶 ZHANG Lanying;ZHANG Fuan;LIU Maomao;CHEN Jie;ZHOU Jian;LIU Yuting;OUYANG Yao(Department of Respiratory and Critical Care Medicine,Affiliated Hospital of Zunyi Medical University,Zunyi 563000,China;Department of Neurosurgery,Affiliated Hospital of Zunyi Medical University,Zunyi 563000,China)

机构地区：[1]遵义医科大学附属医院呼吸与危重症医学科,563000 [2]遵义医科大学附属医院神经外科,563000

出　　处：《天津医药》2024年第9期913-916,共4页Tianjin Medical Journal

基　　金：国家自然科学基金资助项目(82060005);遵义市科技支撑计划项目[遵市科合社字(2018)71,遵市科合HZ字(2021)94号]。

摘　　要：目的 研究CD1a和CD83阳性树突状细胞(DC)在慢性阻塞性肺疾病(COPD)小鼠肺组织中的分布及意义。方法 将20只C57BL/6小鼠采用随机数字表法分为空气对照组和烟熏COPD组,各10例。空气对照组暴露于空气中;烟熏COPD组使用香烟烟熏法建立COPD小鼠模型,于最后一次烟熏结束24 h内处死小鼠,取右下肺。观察2组小鼠体质量变化、肺组织病理变化,测量平均内衬间隔(MLI),免疫组化法检测肺组织中CD1a^(+)、CD83^(+)DC的分布并计数。结果 建模7、14、21、28 d时烟熏COPD组的小鼠体质量较空气对照组均降低(P<0.05);HE染色示烟熏COPD组小鼠肺组织正常肺泡结构破坏,多个肺泡相互融合形成较大的肺泡腔,肺泡间隔有大量炎性细胞浸润,肺泡壁增厚,COPD造模成功;与空气对照组比较,烟熏COPD组MLI值(μm)增大(28.30±3.47 vs. 50.40±3.60),肺组织中CD1a^(+)DC数量(个/视野)增多(9.58±2.18 vs. 17.08±3.67),而CD83^(+)DC数量(个/视野)减少(19.78±4.95 vs. 8.02±3.30),差异有统计学意义(均P<0.05)。结论 烟熏COPD组小鼠肺组织CD1a^(+)DC增多,CD83^(+)DC减少,香烟烟熏可能导致DC成熟障碍。Objective To study the distribution and significance of CD1a and CD83 positive dendritic cells(DCs)in lung tissue of chronic obstructive pulmonary disease(COPD)mice.Methods Twenty C57BL/6 mice were randomly divided into the air control group and the smoked COPD group(n=10 for each group).COPD mouse model was established using cigarette smoking method.Mice were executed within 24 h after the last cigarette smoking,and right lower lung was collected.Body mass changes and lung histopathological changes of mice were observed in two groups.Mean linear intercept(MLI)was measured,and expression levels of CD1a^(+)and CD83^(+)DCs in lung tissue were detected by immunohistochemistry.Results The body mass of mice at 7,14,21 and 28 d after modeling was lower in the smoked COPD group than that in the air control group(P<0.05).HE staining showed that the normal alveolar structure of lung tissue of mice in the smoked group was disrupted,with multiple alveoli fused with each other to form a larger alveolar lumen,a large number of inflammatory cells infiltrated in alveolar intervals,and walls of the alveoli were thickened.COPD modeling was successful.Compared with the air control group,MLI values(µm)increased in the smoked COPD group(28.30±3.47 vs.50.40±3.60),and the number of CD1a^(+)DCs(per field of view)in lung tissue increased(9.58±2.18 vs.17.08±3.67),while the number of CD83^(+)DCs(per field of view)decreased(19.78±4.95 vs.8.02±3.30)(all P<0.05).Conclusion The number of CD1a^(+)DCs in lung tissue is increased and the number of CD83^(+)DCs in lung tissue is decreased in the smoked COPD group of mice,and cigarette smoking may have impaired DC maturation.

关 键 词：肺疾病 慢性阻塞性 树突细胞 吸烟 CD1A CD83 

分 类 号：R563[医药卫生—呼吸系统]