Hoang Laura L, Nguyen Yen P, Aspeé Rayza, Bolton Sarah J, Shen Yi-Hsin, Wang Lei, Kenyon Nicholas J, Smiley-Jewell Suzette, Pinkerton Kent E
1 Center for Health and the Environment, University of California, Davis, California.
2 Respiratory, Inflammation and Autoimmunity Innovative Medicine and Early Development Unit AstraZeneca R&D Mölndal, Mölndal, Sweden; and.
Am J Respir Cell Mol Biol. 2016 Jun;54(6):872-81. doi: 10.1165/rcmb.2015-0119OC.
Airway remodeling is strongly correlated with the progression of chronic obstructive pulmonary disease (COPD). In this study, our goal was to characterize progressive structural changes in site-specific airways, along with the temporal and spatial expression of transforming growth factor (TGF)-β in the lungs of male spontaneously hypertensive rats exposed to tobacco smoke (TS). Our studies demonstrated that TS-induced changes of the airways is dependent on airway generation and exposure duration for proximal, midlevel, and distal airways. Stratified squamous epithelial cell metaplasia was evident in the most proximal airways after 4 and 12 weeks but with minimal levels of TGF-β-positive epithelial cells after only 4 weeks of exposure. In contrast, epithelial cells in midlevel and distal airways were strongly TGF-β positive at both 4 and 12 weeks of TS exposure. Airway smooth muscle volume increased significantly at 4 and 12 weeks in midlevel airways. Immunohistochemistry of TGF-β was also found to be significantly increased at 4 and 12 weeks in lymphoid tissues and alveolar macrophages. ELISA of whole-lung homogenate demonstrated that TGF-β2 was increased after 4 and 12 weeks of TS exposure, whereas TGF-β1 was decreased at 12 weeks of TS exposure. Airway levels of messenger RNA for TGF-β2, as well as platelet-derived growth factor-A, granulocyte-macrophage colony-stimulating factor, and vascular endothelial growth factor-α, growth factors regulated by TGF-β, were significantly decreased in animals after 12 weeks of TS exposure. Our data indicate that TS increases TGF-β in epithelial and inflammatory cells in connection with airway remodeling, although the specific role of each TGF-β isoform remains to be defined in TS-induced airway injury and disease.
气道重塑与慢性阻塞性肺疾病(COPD)的进展密切相关。在本研究中,我们的目标是描述特定部位气道的渐进性结构变化,以及暴露于烟草烟雾(TS)的雄性自发性高血压大鼠肺中转化生长因子(TGF)-β的时空表达。我们的研究表明,TS诱导的气道变化取决于气道分级以及近端、中级和远端气道的暴露持续时间。4周和12周后,最近端气道出现明显的分层鳞状上皮化生,但仅暴露4周后,TGF-β阳性上皮细胞水平最低。相比之下,在TS暴露4周和12周时,中级和远端气道的上皮细胞TGF-β呈强阳性。中级气道在4周和12周时气道平滑肌体积显著增加。在4周和12周时,淋巴组织和肺泡巨噬细胞中TGF-β的免疫组化也显著增加。全肺匀浆的ELISA显示,TS暴露4周和12周后TGF-β2增加,而TS暴露12周时TGF-β1减少。TS暴露12周后,动物气道中TGF-β2以及血小板衍生生长因子-A、粒细胞-巨噬细胞集落刺激因子和血管内皮生长因子-α(这些生长因子受TGF-β调节)的信使RNA水平显著降低。我们的数据表明,TS与气道重塑相关,可增加上皮细胞和炎症细胞中的TGF-β,尽管每种TGF-β异构体在TS诱导的气道损伤和疾病中的具体作用仍有待确定。