Abstract
The clinical characteristics of asthma can be logically explained by asthma-specific airway inflammation and airway remodeling, the details of which have been recently elucidated. Airway remodeling is an important feature of chronic airway disease, but the mechanisms involved remain unclear.
Since TGF-b has been implicated in the development of airway remodeling in asthma based on its strong capacity to induce extracellular matrix (ECM) production, it is possible that Smad7 may also play some roles in the regulation of the process.
Method: We analyzed using by real time RT-PCR and Western blotting method.We thought to determine the relationships between Collagen type I production in normal human bronchial cell line (NHBE).
Normal human bronchial epithelial cells (NHBE) cells stimulated with Th2 type cytokine TGF-beta or regulately cytokine IL-10. Production levels of Type I collagen was expressed in cultured epithelial cells NHBE stimulation with TGF-b.
Furthermore, collagen type I production in NHBE cells stimulation with TGF-b up-regulate in a dose and time dependent manner. And also we found that protein levels of collagen type I were increased from activated NHBE cells stimulating with TGF-b.
In contrast, IL-10 decreased collagen type I expression in NHBE cells.
In conclusion, these findings suggested bronchial epithelial cells may produce collagen type I production and IL-10 is a key cytokine possible make an important role of airway remodeling.
- © 2011 ERS
