Division of Pulmonary, Allergy & Critical Care Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Allergy. 2012 Dec;67(12):1601-4. doi: 10.1111/all.12021. Epub 2012 Sep 25.
Caveolin-1 has emerged as a critical regulator of signaling pathways involved in lung fibrosis and inflammation.
Therefore, we investigated whether caveolin-1 is deficient in asthmatic patients and in a murine model of asthma.
Immunohistochemical analyses of endobronchial biopsies showed a remarkable loss of caveolin-1 in the lungs of asthmatic patients compared with controls. This loss was most evident in bronchial epithelial cells and associated with an increase in the expression of extracellular matrix proteins: collagen I, tenascin, and periostin. Cultured primary bronchial epithelial cells of asthmatics had lower caveolin-1 expression compared with control cells. In addition, caveolin-1 expression was significantly decreased in peripheral blood monocytes from asthma patients. The loss of caveolin-1 was also observed in a mouse model for asthma (mice sensitized and challenged with aspergillus fumigatus).
To our knowledge, this is the first demonstration that the regulatory protein caveolin-1 is reduced in patients with asthma.
小窝蛋白-1 已成为参与肺纤维化和炎症的信号通路的关键调节因子。
因此,我们研究了哮喘患者和哮喘小鼠模型中是否存在小窝蛋白-1 缺乏的情况。
对支气管内膜活检的免疫组织化学分析表明,与对照组相比,哮喘患者肺组织中的小窝蛋白-1明显缺失。这种缺失在支气管上皮细胞中最为明显,并伴有细胞外基质蛋白(I 型胶原、腱糖蛋白和骨桥蛋白)表达增加。与对照细胞相比,哮喘患者的原代支气管上皮细胞中表达的小窝蛋白-1较低。此外,哮喘患者外周血单核细胞中的小窝蛋白-1表达也显著降低。在哮喘的小鼠模型中也观察到小窝蛋白-1的缺失(用烟曲霉致敏和激发的小鼠)。
据我们所知,这是首次证明哮喘患者的调节蛋白小窝蛋白-1减少。