YKL-40-induced IL-8 expression from bronchial epithelium leads to bronchial smooth muscle proliferation and migration
10.3969/j.issn.1000-484X.2014.12.002
- VernacularTitle:YKL-40调控支气管上皮分泌 IL-8对支气管平滑肌细胞增殖和迁移的影响
- Author:
Lin XIAO
;
Zhaoquan SHI
;
Bing LI
;
Qingyu XIU
;
Hao TANG
- Publication Type:Journal Article
- Keywords:
YKL-40;
Bronchial epithelial cell;
IL-8;
Bronchial smooth muscle cell
- From:
Chinese Journal of Immunology
2014;(12):1591-1595
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate YKL-40-mediated inflammation in human bronchial epithelial cells and analyzed the soluble factors secreted by bronchial epithelial cells exposed to YKL-40 that were responsible for increasing proliferation and migration of primary normal human bronchial smooth muscle cells (BSMCs).Methods:YKL-40-induced inflammation was assayed in two human bronchial epithelial cells (BEAS-2B cell line and primary human bronchial epithelial cells ,namely HBECs).In addition,we treated BEAS-2B cells and HBECs with YKL-40,and added the conditioned culture media ( YKL-40-BEAS-2B-CM) and ( YKL-40-HBECs-CM) to BSMCs.The proliferation and migration of BSMCs were determined by premixed WST-1 cell proliferation reagent and QCM chemotaxis migration assay ,respectively.Results: Bronchial epithelial cells treated with YKL-40 resulted in a significant increase of IL-8 production,but have no effect about RANTES ,Eotaxin and TNF-α.YKL-40-BEAS-2B-CM and YKL-40-HBECs-CM induced IL-8 was found to further stimulate proliferation and migration of BSMCs ,and the effects were inhibited after neutralizing IL-8.Conclusion:Through investigating the interaction of airway epithelium and smooth muscle ,our findings implicate that YKL-40 may be involved in the inflammation of asthma by induction of IL-8 from epithelium,subsequently contributing to BSMCs proliferation and migration.Moreover, inhibition of IL-8 signaling is a potential therapeutic target for YKL-40-induced inflammation and remodeling of asthma.
