慢阻肺大鼠肺组织中树突状细胞表面因子的表达变化及CCL20抗体的干预作用

发布时间：2018-10-31 10:35

【摘要】：目的了解树突状细胞表面因子OX62、CD83在慢阻肺大鼠肺部的表达变化,并探讨CCL20抗体的干预作用。方法选用30只健康Wistar大鼠,随机分为健康对照组(10只)、慢阻肺模型组(10只)、CCL20单抗组(10只),用气道内注入脂多糖(共2次)联合烟雾刺激(约28 d)的方法诱导慢阻肺模型。在实验初始对单抗组大鼠以CCL20单克隆抗体腹腔注射一次。在第29天取大鼠的肺组织观察其病理学改变,用免疫组织化学技术检测肺部树突状细胞(DC)的表面因子OX62、CD83的表达变化。结果模型组大鼠肺组织HE染色符合气道炎症和肺气肿的表现,CCL20单抗组大鼠肺部病理表现比慢阻肺组明显减轻。与健康对照组相比,慢阻肺模型组大鼠的肺组织中OX62的表达比对照组明显增多(P0.05),而在CCL20单抗组低于慢阻肺组(P0.05)。慢阻肺模型组大鼠肺组织中CD83的表达比对照组少(P0.05),而在慢阻肺组与CCL20单抗组之间则没有明显的差异(P0.05)。结论慢阻肺的发病可能与肺部OX62的表达增多及CD83的表达减少有关,使用CCL20单抗能部分地抑制这一效应。
[Abstract]:Objective to investigate the expression of dendritic cell surface factor (OX62,CD83) in lung of COPD rats and to explore the effect of CCL20 antibody. Methods Thirty healthy Wistar rats were randomly divided into control group (n = 10), chronic obstructive pulmonary model group (n = 10) and CCL20 monoclonal antibody group (n = 10). The model of chronic obstructive lung was induced by intratracheal injection of lipopolysaccharide (2 times) combined with smoke stimulation (about 28 days). At the beginning of the experiment, the rats in the monoclonal antibody group were injected intraperitoneally with CCL20 monoclonal antibody. The pathological changes of lung tissue were observed on the 29th day, and the expression of surface factor OX62,CD83 of (DC) in dendritic cells was detected by immunohistochemistry. Results HE staining in lung tissue of model group was consistent with the manifestations of airway inflammation and emphysema. The pathological manifestations of lung in CCL20 monoclonal antibody group were significantly less than those in slow obstructive lung group. Compared with the healthy control group, the expression of OX62 in the lung tissue of the COPD model group was significantly higher than that of the control group (P0.05), while the expression of OX62 in the CCL20 monoclonal antibody group was lower than that in the COPD group (P0.05). The expression of CD83 in the lung tissue of the COPD model group was lower than that of the control group (P0.05), but there was no significant difference between the COPD group and the CCL20 monoclonal antibody group (P0.05). Conclusion the pathogenesis of COPD may be related to the increase of OX62 expression and the decrease of CD83 expression, which can be partly inhibited by the use of CCL20 monoclonal antibody.
【作者单位】：遵义医学院附属医院呼吸一科;华中科技大学同济医学院附属同济医院呼吸与危重症医学科卫生部呼吸系统疾病重点实验室;
【基金】：国家自然科学基金(81460008)
【分类号】：R563.9

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