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作 者:张婧 张兰英 欧阳瑶 Zhang Jing;Zhang Lanying;Ouyang Yao(Department of Pulmonary and Critical Care Medicine,the Affiliated Hospital of Zunyi Medical University,Zunyi Guizhou 563099,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,贵州遵义563099
出 处:《遵义医科大学学报》2022年第4期457-462,共6页Journal of Zunyi Medical University
基 金:国家自然科学基金资助项目(NO:81460008);遵义医学院硕士启动资金资助项目(NO:院字[2016]58)。
摘 要:目的通过检测慢性阻塞性肺疾病(COPD)小鼠外周血和支气管肺泡灌洗液(BALF)中树突状细胞(DC)表面标记物CD83及辅助性T细胞17(Th17)、调节性T细胞(Treg)的表达并进一步分析其意义,以期丰富COPD的免疫发病机制。方法SPF级C57BL/6小鼠随机分为对照组(Control组)(n=10)和COPD模型组(n=16)。采用烟熏的方法构建COPD小鼠模型。实验第28天处死两组小鼠,收集小鼠的外周血、肺组织和BALF。通过HE染色观察肺组织的病理变化。流式细胞术检测外周血和BALF中CD83、Th17及Treg的表达。结果(1)与Control组相比,COPD模型组小鼠肺组织可见明显的炎症细胞浸润及肺气肿形成;(2)与Control组相比,COPD模型组小鼠外周血和BALF中CD83表达降低(P<0.05);(3)与Control组相比,COPD模型组小鼠外周血和BALF中Th17细胞产生增多(P<0.05);(4)与Control组相比,COPD模型组小鼠外周血和BALF中Treg细胞产生减少(P<0.05);(5)与Control组相比,COPD模型组小鼠外周血和BALF中Th17/Treg细胞比例升高。结论香烟烟雾可能阻碍DC成熟,CD83^(+)DC可能参与COPD的发病;香烟烟雾可能通过阻碍DC成熟而导致Th17/Treg细胞失衡,从而参与COPD的发生发展。Objective To detect the expression of CD83 and Th17/Treg cells in peripheral blood and bronchoalveolar lavage fluid(BALF)of mice with chronic obstructive pulmonary disease(COPD)and analyze their significance.Methods C57BL/6 mice were randomly divided into control group(control)(n=10)and COPD model group(n=16).Exposure to cigarette-smoking was used to establish the mice model of COPD.At day 28,mice in two groups were sacrificed and the lung tissues,peripheral blood and BALF were collected.HE staining was performed to observe the pathological changes of mice lung tissue.The expression of CD83,Th17 and Treg in peripheral blood and BALF was detected by flow cytometry.Results(1)Compared with control group,pulmonary inflammation and formation of emphysema were increased in the lung tissue of COPD model group;(2)Compared with the control group,the percentage of CD83 in COPD model group was decreased in the peripheral blood and BALF;(3)Compared with the control group,the percentage of Th17 in the peripheral blood and BALF in COPD model group was increased;(4)Compared with control group,the percentage of Treg in COPD model group was decreased;(5)The ratio of Th17/Treg in the peripheral blood and BALF in COPD model group was higher than that in the control group.Conclusion(1)Cigarette smoke could suppress the normal dendritic cell(DC)maturation and CD83^(+)DC might play an important role in the pathogenesis of COPD;(2)Cigarette smoke might lead to the imbalance of Th17/Treg via inhibiting DC maturation,which could be involved in the occurrence and development of COPD.
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