β2 adrenergic agonist suppresses eosinophil-induced epithelial-to-mesenchymal transition of bronchial epithelial cells

Respiratory Research

Research

Mizuho Nagao¹  Takao Fujisawa¹  Koa Hosoki²  Yu Kuwabara²  Keigo Kainuma²  Corina N. D’Alessandro-Gabazza³  Masaaki Toda³  Taro Yasuma³  Kota Nishihama³  Esteban C. Gabazza³  Hajime Fujimoto⁴  Tetsu Kobayashi⁴ 

[1] Allergy Center, Mie National Hospital, 357 Osato-kubota, 514-0125, Tsu, Mie, Japan;Allergy Center, Mie National Hospital, 357 Osato-kubota, 514-0125, Tsu, Mie, Japan;Department of Immunology, Mie University Graduate School of Medicine, Edobashi 2-174, 514-8507, Tsu, Mie, Japan;Department of Immunology, Mie University Graduate School of Medicine, Edobashi 2-174, 514-8507, Tsu, Mie, Japan;Department of Pulmonary and Critical Care Medicine, Mie University Graduate School of Medicine, Edobashi 2-174, 514-8507, Tsu, Mie, Japan;

关键词: Asthma;    Eosinophils;    Epithelial cells;    Integrins;   

DOI  :  10.1186/s12931-017-0563-4

 received in 2017-02-26, accepted in 2017-04-25,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundEpithelial-mesenchymal transition is currently recognized as an important mechanism for the increased number of myofibroblasts in cancer and fibrotic diseases. We have already reported that epithelial-mesenchymal transition is involved in airway remodeling induced by eosinophils. Procaterol is a selective and full β2 adrenergic agonist that is used as a rescue of asthmatic attack inhaler form and orally as a controller. In this study, we evaluated whether procaterol can suppress epithelial-mesenchymal transition of airway epithelial cells induced by eosinophils.MethodsEpithelial-mesenchymal transition was assessed using a co-culture system of human bronchial epithelial cells and primary human eosinophils or an eosinophilic leukemia cell line.ResultsProcaterol significantly inhibited co-culture associated morphological changes of bronchial epithelial cells, decreased the expression of vimentin, and increased the expression of E-cadherin compared to control. Butoxamine, a specific β2-adrenergic antagonist, significantly blocked changes induced by procaterol. In addition, procaterol inhibited the expression of adhesion molecules induced during the interaction between eosinophils and bronchial epithelial cells, suggesting the involvement of adhesion molecules in the process of epithelial-mesenchymal transition. Forskolin, a cyclic adenosine monophosphate-promoting agent, exhibits similar inhibitory activity of procaterol.ConclusionsOverall, these observations support the beneficial effect of procaterol on airway remodeling frequently associated with chronic obstructive pulmonary diseases.

【 授权许可】

CC BY   
© The Author(s). 2017