Department of Allergy, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Allergy Asthma Immunol Res. 2010 Jan;2(1):41-7. doi: 10.4168/aair.2010.2.1.41. Epub 2009 Dec 30.
Chlamydophila pneumoniae infection in the airways is thought to be associated with the pathogenesis of asthma, especially in non-atopic severe asthma with irreversible airway obstruction that may be related to airway remodeling. Here, we investigated whether C. pneumoniae infection enhances the secretion of critical chemical mediators for airway remodeling, such as VEGF, TGF-beta, and TIMP-1, in human bronchial epithelial cells (BECs) in a Th2-dominant microenvironment.
Human bronchial epithelial cells (BEAS-2B cells) were infected with C. pneumoniae strain TW183 and cultured in both a Th1-dominant microenvironment with INF-gamma and a Th2-dominant microenvironment with IL-4 or IL-13 added to the culture medium. The VEGF, TGF-beta, and TIMP-1 levels in the culture supernatants were measured using enzyme-linked immunosorbent assays (ELISA). The activation of NF-kappaB in each experimental condition was determined using an electrophoretic mobility shift assay.
Chlamydophila pneumoniae-infected BECs showed enhanced secretion of VEGF, TGF-beta, and TIMP-1 compared with non-infected BECs. The levels of cytokines secreted from BECs were increased more when IL-13 was added to the culture medium. C. pneumoniae-infected BECs also showed increased NF-kappaB activation.
These results suggest that C. pneumoniae plays a role in the pathogenesis of airway remodeling in asthma, revealing a Th2-dominant immune response. Further studies are required to clarify the precise mechanism of C. pneumoniae infection in airway remodeling.
人们认为，呼吸道沙眼衣原体（Chlamydophila pneumoniae）感染与哮喘的发病机制有关，尤其是在非特应性严重哮喘中，这种感染与不可逆的气道阻塞有关，而气道重构可能与之相关。在此，我们研究了在 Th2 优势型微环境中，衣原体感染是否会增强人支气管上皮细胞（BEC）中关键的气道重构化学介质的分泌，如 VEGF、TGF-β 和 TIMP-1。
用沙眼衣原体 TW183 株感染人支气管上皮细胞（BEAS-2B 细胞），并在 IFN-γ诱导的 Th1 优势型微环境和加入培养基的 IL-4 或 IL-13 诱导的 Th2 优势型微环境中进行培养。使用酶联免疫吸附试验（ELISA）测量培养上清液中的 VEGF、TGF-β 和 TIMP-1 水平。通过电泳迁移率变动分析测定各实验条件下 NF-κB 的激活情况。
与未感染的 BEC 相比，感染沙眼衣原体的 BEC 显示出增强的 VEGF、TGF-β 和 TIMP-1 分泌。当向培养基中加入 IL-13 时，BEC 分泌的细胞因子水平增加更多。感染沙眼衣原体的 BEC 也显示 NF-κB 激活增加。
这些结果表明，衣原体在哮喘气道重构的发病机制中起作用，揭示了 Th2 优势型免疫反应。需要进一步的研究来阐明衣原体感染在气道重构中的精确机制。
