| | | 肺表面活性物质对哮喘小鼠模型树突细胞功能的调节机制
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Role of pulmonary surfactant in regulating dendritic cell function of murine asthma models
【Abstract】 AIM: To explore the mechanisms of exogenous pulmonary surfactant（PS） in regulating the immunity of murine asthma models and its effect on dendritic cell (DC) function of the spleen of the asthma models. METHODS: Murine asthma models were established with ovalbumin (OVA) sensitization and challenge and the models were confirmed by histological analysis of lung tissues. FACS was used to measure the expression of CD80 on DC derived from the spleen of OVAsensitized and challenged mice. PS was inhaled after OVA challenge by 20 g/L for 2, 5, 10, 15 and 20 min. IL12 in DC culture medium was tested at 2, 4, 6, 12 and 24 h and data were analyzed with SPSS 10.0 software. RESULTS: Histological analysis results of lung tissues were consistent with the characteristics of murine asthma model. The expression rate of CD80 on spleenderived DC in asthma group significantly increased compared with that in PS group (P<0.01) and CD80 expression rate was the lowest when PS was inhaled for 2 min. IL12 in asthma group decreased compared with that in PS group (P<0.01). PS group kept IL12 at a high level for a long time while IL12 expression level was low and lasted for a short time in asthma group. CONCLUSION: Abnormal DC function is existent in murine asthma models and exogenous surfactant can regulate the DC function by suppressing the expression of CD80 on DC and increasing the level of IL12 secreted by DC, which can improve the respiratory function when the asthma is challenged.
【Keywords】 pulmonary surfactant； dendritic cell； costimulatory molecules；IL12； asthma
【摘要】 目的免费论文下载： 研究外源性肺表面活性物质对小鼠哮喘模型的免费论文下载免疫调节作用及其对树突细胞（DC）功能的影响. 方法：BALB/c小鼠50只，分为3组：哮喘组15只［采用卵蛋白（OVA）致敏和激发］、对照组15只（以生理盐水代替OVA致敏和激发）、治疗组20只［每次OVA激发后10 min以肺表面活性物质（PS） 20 g/L雾化吸入，时间为2,5,10,15和20 min］. 用HE染色方法评定哮喘模型. 分离培养脾脏DC，用流式细胞仪（FACS）检测DC表面共刺激分子CD80的表达变化. 取DC培养液3 mL，加入OVA，调整OVA浓度至10 mg/L. 分别在2，4，6，12，24 h取DC培养液，1300 r/min离心5 min，取上清液，ELISA法检测IL12 P70. 结果： 哮喘组小鼠的肺组织表现为嗜酸细胞及淋巴细胞浸润为主的炎症变化，治疗组和对照组无此变化. 哮喘组DC阳性表达率明显高于治疗组(P<0.01)；吸入PS对DC表面共刺激分子的抑制作用在2 min时最强. 哮喘组DC上清液IL12低于治疗组(P<0.01)；治疗组DC上清液IL12可以在高水平维持较长时间，而哮喘组的DC上清液IL12含量降低，且维持时间较短. 结论：小鼠哮喘模型中存在明显的DC功能缺陷；外源性吸入PS，能明显改善DC功能，从而保护哮喘发作时小鼠的肺功能.
【关键词】 肺表面活性剂；树突细胞；共刺激分子；白细胞介素12；哮喘
0引言
支气管哮喘(简称哮喘)是一种慢性气道炎症,其中CD4+ T淋巴细胞异常活化起关键作用. 肺表面活性物质(pulmonary surfactant，PS)是由肺泡Ⅱ型细胞合成、分泌的脂蛋白,具有降低表面张力、维持肺泡稳定性作用. 研究表明,哮喘发作时气道中的PS存在量和功能的异常［1］,从而加重气道阻塞,而外源性补充PS可明显减轻症状，改善肺功能. 体外研究发现, PS的脂质成分具有抗炎及免疫调节作用［2］. 树突状细胞(dendritic cell，DC)是体内强有力的专职抗原提呈细胞. DC通过MHC和共刺激分子与Th0相互作用，提呈抗原给T淋巴细胞(TC)，并通过产生细胞因子(如IL12)诱导Th1或Th2型免疫. IL12可诱导强烈的Th1应答反应，其在维持Th1/Th2平衡方面起关键作用［3］ . 我们从外源性吸入肺表面活性物质调节DC功能方面探讨其治疗支气管哮喘的免疫学机制.
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