孟鲁卡斯特
上皮-间质转换
嗜酸性粒细胞
白三烯受体
免疫学
细胞培养
癌症研究
化学
医学
哮喘
下调和上调
生物
生物化学
遗传学
基因
作者
Koa Hosoki,Keigo Kainuma,Masaaki Toda,Eijiro Harada,Ayshwarya-Lakshmi Chelakkot-Govindalayathila,Ziaurahman Roeen,Mizuho Nagao,Corina N. D’Alessandro-Gabazza,Takao Fujisawa,Esteban C. Gabazza
标识
DOI:10.1016/j.bbrc.2014.05.033
摘要
Epithelial to mesenchymal transition (EMT) is a mechanism by which eosinophils can induce airway remodeling. Montelukast, an antagonist of the cysteinyl leukotriene receptor, can suppress airway remodeling in asthma. The purpose of this study was to evaluate whether montelukast can ameliorate airway remodeling by blocking EMT induced by eosinophils. EMT induced was assessed using a co-culture system of human bronchial epithelial cells and human eosinophils or the eosinophilic leukemia cell lines, Eol-1. Montelukast inhibited co-culture associated morphological changes of BEAS-2b cells, decreased the expression of vimentin and collagen I, and increased the expression of E-cadherin. Montelukast mitigated the rise of TGF-β1 production and Smad3 phosphorylation. Co-culture of human eosinophils with BEAS-2B cells significantly enhanced the production of CysLTs compared with BEAS-2B cells or eosinophils alone. The increase of CysLTs was abolished by montelukast pre-treatment. Montelukast had similar effects when co-culture system of Eol-1 and BEAS-2B was used. This study showed that montelukast suppresses eosinophils-induced EMT of airway epithelial cells. This finding may explain the mechanism of montelukast-mediated amelioration of airway remodeling in bronchial asthma.
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