Transforming growth factor-β2 induces bronchial epithelial mucin expression in asthma
Transforming growth factor-β2 induces bronchial epithelial mucin expression in asthma
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DOI：
10.1016/s0002-9440(10)63371-8
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发表时间：
2004-10-01
影响因子：
6
通讯作者：
Wenzel, SE
中科院分区：
文献类型：
--
作者：
Chu, HW;Balzar, S;Wenzel, SE
转化生长因子（TGF）-β家族对于包括哮喘在内的病理状况中的组织修复是重要的。然而，关于TGF-β 1或TGF-β 2对哮喘气道上皮粘蛋白表达的影响知之甚少。我们评估了支气管上皮TGF-β 1和TGF-β 2的表达及其对粘蛋白表达的影响，以及TGF-β 1或TGF-β 2在白细胞介素（IL）-13诱导的粘蛋白表达中的作用。在哮喘患者和正常人的支气管内活检中评估了上皮TGF-β 1、TGF-β 2和粘蛋白的表达。在来自两个受试者组支气管内刷拭的培养支气管上皮细胞中确定了TGF-β 1或TGF-β 2对粘蛋白MUC 5AC蛋白和mRNA表达的影响，以及IL-13对上皮TGF-β 1、TGF-β 2和MUC 5AC的影响。在活检组织中，哮喘患者和正常人的上皮TGF-β 2表达水平均高于TGF-β 1。与正常人相比，哮喘患者TGF-β 2升高，而TGF-β 1没有升高，并且与粘蛋白表达显著相关。TGF-β 2，而不是TGF-β 1，增加了两个受试者组培养的上皮细胞中的粘蛋白表达。IL-13增加了上皮细胞TGF-β 2的释放，但不增加TGF-β 1的释放。中和TGF-β 2抗体部分抑制IL-13诱导的粘蛋白表达。这些数据表明，哮喘支气管上皮细胞产生TGF-β 2可能增加气道粘蛋白表达。IL-13诱导的粘蛋白表达可能部分通过TGF-β 2上调发生。
The transforming growth factor (TGF)-beta family is important for tissue repair in pathological conditions including asthma. However, little is known about the impact of either TGF-beta1 or TGF-beta2 on asthmatic airway epithelial mucin expression. We evaluated bronchial epithelial TGF-beta1 and TGF-beta2 expression and their effects on mucin expression, and the role of TGF-beta1 or TGF-beta2 in interleukin (IL)-13-induced mucin expression. Epithelial TGF-beta1, TGF-beta2, and mucin expression were evaluated in endobronchial biopsies from asthmatics and normal subjects. The effects of TGF-beta1 or TGF-beta2 on mucin MUC5AC protein and mRNA expression, and the impact of IL-13 on epithelial TGF-beta1, TGF-beta2, and MUC5AC were determined in cultured bronchial epithelial cells from endobronchial brushings of both subject groups. In biopsy tissue, epithelial TGF-beta2 expression levels were higher than TGF-beta1 in both asthmatics and normals. TGF-beta2, but not TGF-beta1, was increased in asthmatics compared with normals, and significantly correlated with mucin expression. TGF-beta2, but not TGF-beta1, increased mucin expression in cultured epithelial cells from both subject groups. IL-13 increased the release of TGF-beta2, but not TGF-beta1, from epithelial cells. A neutralizing TGF-beta2 antibody partially inhibited IL-13-induced mucin expression. These data suggest that TGF-beta2 production by asthmatic bronchial epithelial cells may increase airway mucin expression. IL-13-induced mucin expression may occur in part through TGF-beta2 up-regulation.