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本研究探讨mTSLPR-Ig逆转哮喘小鼠Th1/Th2失衡以及改善哮喘气道炎症的可行性及其诱导哮喘免疫耐受的机制。实验包括用卵白蛋白(OVA)腹腔注射致敏和雾化吸入激发BALB/c小鼠,建立哮喘动物模型。于OVA激发前,将mTSLPR-Ig进行小鼠滴鼻灌注,光镜下对BALF中细胞总数及嗜酸粒细胞、淋巴细胞进行计数;ELISA法检测BALF中细胞因子IL-4、IL-5、IFN-γ以及IL-10水平;HE组织染色法观察小鼠肺部炎症表现。分离小鼠肺脏并制备成细胞悬液,FCM检测肺脏CD11c+细胞表面共刺激分子CD80、CD86以及CD40的表达变化。结果表明,mTSLPR-Ig治疗组与哮喘组比较,BALF中细胞总数和嗜酸粒细胞计数显著减少(P<0.01)、BALF中IL-4、IL-5水平均显著降低(P<0.01),而IL-10、IFN-γ显著升高(P<0.01);小鼠肺部炎症明显减轻。mTSLPR-Ig治疗组肺脏CD11 c+细胞表面分子CD80、CD86以及CD40较哮喘组显著降低。mTSLPR-Ig能显著抑制哮喘小鼠Th1/Th2失衡以及肺部变应性炎症,该效应可能与mTSLPR-Ig抑制肺脏CD11 c+细胞共刺激分子表达有关。mTSLPR-Ig对哮喘的治疗具有重要的潜在临床应用价值,为哮喘的治疗提供了可能的新途径。
This study was aimed to investigate whether mTSLPR-Ig reverses the imbalance of Th1 / Th2 in asthmatic mice and improves the airway inflammation in asthmatic mice and the mechanism of its induction of immune tolerance. The experiment included BALB / c mice challenged by intraperitoneal injection of ovalbumin (OVA) and inhalation by atomization to establish an animal model of asthma. Before OVA challenge, mTSLPR-Ig was intranasally instilled into mice, and the total number of BALF cells, eosinophils and lymphocytes were counted under light microscope. The levels of IL-4, IL-5, IFN-γ and IL-10 levels; HE staining of the lungs to observe the performance of mice. The lungs of mice were isolated and prepared into cell suspension. The expression of costimulatory molecules CD80, CD86 and CD40 on the surface of lung CD11c + cells were detected by FCM. The results showed that the total number of cells and the number of eosinophils in BALF were significantly decreased (P <0.01) and the levels of IL-4 and IL-5 in BALF were significantly decreased in mTSLPR-Ig treatment group compared with asthma group (P <0.01) While the levels of IL-10 and IFN-γ were significantly increased (P <0.01). The lung inflammation in mice was significantly reduced. MTSLPR-Ig treatment group lung CD11 c + cell surface molecules CD80, CD86 and CD40 significantly lower than the asthma group. mTSLPR-Ig can significantly inhibit the imbalance of Th1 / Th2 and allergic inflammation of lung in asthmatic mice. This effect may be related to the inhibition of mTSLPR-Ig expression of costimulatory molecules in lung CD11 c + cells. mTSLPR-Ig has important potential clinical value for the treatment of asthma, which provides a new possible way for the treatment of asthma.