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KMID : 1225720100020010041
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Allergy, Asthma & Immunology Research : AAIR
2010 Volume.2 No. 1 p.41 ~ p.47
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Chlamydophila pneumoniae enhances secretion of VEGF, TGF-β and TIMP-1 from human bronchial epithelial cells under Th2 dominant microenvironment
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Park Chan-Sun
Kim Tae-Bum
Bae Yun-Jeong
Lee Hee-Ran
Moon Hee-Bom
Cho You-Sook
Moon Keun-Ae
Jang Min-Kyoung
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Abstract
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Purpose: 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-β, and TIMP-1, in human bronchial epithelial cells (BECs) in a Th2-dominant microenvironment.
Methods: Human bronchial epithelial cells (BEAS-2B cells) were infected with C. pneumoniae strain TW183 and cultured in both a Th1-dominant microenvironment with INF-γ and a Th2-dominant microenvironment with IL-4 or IL-13 added to the culture medium. The VEGF, TGF-β, and TIMP-1 levels in the culture supernatants were measured using enzyme-linked immunosorbent assays (ELISA). The activation of NF-κB in each experimental condition was determined using an electrophoretic mobility shift assay.
Results: Chlamydophila pneumoniae-infected BECs showed enhanced secretion of VEGF, TGF-β, 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-κB activation.
Conclusions: 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.
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KEYWORD
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Asthma, Chlamydophila pneumonia, epithelial cells, vascular endothelial growth factor A, tissue inhibitor of metalloproteinases, transforming growth factor beta
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