小鼠哮喘模型胸腺中胸腺基质淋巴生成素、Foxp3的表达及调节

目的通过建立小鼠哮喘模型，探讨胸腺在过敏性疾病发病机制中的作用，以及胸腺肽干预哮喘模型的作用和可能的机制。方法40只小鼠随机分为哮喘模型组、卵清蛋白（OVA）＋胸腺肽组、对照组和胸腺肽组，每组各10只。①采用OVA腹腔注射和超声雾化吸入建立BALB/c小鼠哮喘模型；②通过血清总IgE水平和肺组织病理学检查评价哮喘模型；③用Real time PCR检测哮喘模型和胸腺肽干预下，小鼠肺组织和胸腺中胸腺基质淋巴生成素（TSLP）以及胸腺Foxp3 mRNA表达变化，并通过血清总IgE水平和肺组织病理学评价胸腺肽干预下哮喘模型的过敏状态。结果①哮喘模型组与对照组相比，血清总IgE浓度明显增高，肺组织病理学检查示气道炎症明显，胸腺和肺组织TSLP mRNA表达均显著增高，胸腺Foxp3 mRNA表达显著降低；②OVA＋胸腺肽组肺组织病理学检查示气道炎症减轻，胸腺TSLP mRNA表达显著低于哮喘模型组。结论 ①OVA哮喘模型胸腺TSLP mRNA的表达水平上调、Foxp3 mRNA的表达水平下调，提示OVA可影响中枢性免疫器官--胸腺；②OVA哮喘模型引起胸腺Foxp3 mRNA表达降低，提示胸腺功能的改变可能与过敏性疾病的发生有关；③胸腺肽可改善过敏状况，其作用机制至少部分是通过胸腺而发挥。

Expression and modulation of TSLP, Foxp3 in central immune organ (thymus) in mice asthma model

ObjectiveMice asthma model was employed to investigate the role of thymus on the mechanism of the development of allergic diseases. Meanwhile,thymosin was used as an intervention, and the effects and underlying mechanisms of thymosin in allergy therapies were studied. MethodsForty mice were randomly divided into four groups(n=10):asthma model group, OVA+thymosin group, control group and thymosin group.①Establishment of BALB/c mice asthma model: Mice were sensitized by intraperitoneal injection of OVA and airway was challenged by ultrasonic atomizing inhalation of OVA. ②Mice model was evaluated by serum total IgE and lung histopathology. ③Detection of expressions of TSLP, Foxp3 in thymus and TSLP in lung in asthma group and OVA+thymosin group by real time PCR.Results①Serum level of IgE in asthma model group was higher than that in control group（P<0.05）; Histological analysis demonstrated more severe inflammatory reactions in lungs of asthma model group than that of control group. In asthma model group, the mRNA expression level of TSLP in thymus was significant higher than that in the control group（P<0.01）, expression level of TSLP in lungs was higher than that in control group（P<0.05）, expression level of Foxp3 in thymus was lower than that in control group（P<0.05）. ②Inflammatory changes in lungs of OVA+ thymosin group were much better than those in the asthma model group. The mRNA expression level of TSLP in thymus in asthma model group and thymosin group was significant lower than that in asthma model group（P<0.01）Conclusions①Increased TSLP expression and deceased Foxp3 expression suggested that sensitization itself could influence thymus. ②The changes of the expression of Foxp3 in thymus implied that the relationship of thymus with the onset of OVA induced asthma. ③Thymosin may reverse sensitization by downregulating expression of TSLP in thymus. It suggested that the mechanism of thymosin in allergy therapy was partially by influencing thymus function.