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Volume 40, Number 5, October 2007

Comparison of the effects of two long-acting beta2-agonists on cytokine secretion by human airway epithelial cells

Jou-Chia Chiu, Jeng-Yuan Hsu, Lin-Shien Fu, Jao-Jia Chu, Chin-Shiang Chi
Division of Immunology and Nephrology, Department of Pediatrics, and 2Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan

Received: May 4, 2006    Revised: August 27, 2006    Accepted: September 11, 2006   


Corresponding author:

Dr. Lin-Shien Fu, Department of Pediatrics, Taichung Veterans General Hospital, No. 160, Section 3, Chung-Kang Road, Taichung 40705, Taiwan. E-mail: Dr. Lin-Shien Fu This e-mail address is being protected from spam bots, you need JavaScript enabled to view it



Background and purpose: 

Long-acting beta2-agonists (LABAs) have proved to be useful in the management of asthma and prevention of exacerbations. LABAs can modulate inflammatory and repair processes in the airways of individuals affected by many respiratory disorders. This study assessed the effects of LABAs on the release of inflammatory mediators by bronchial epithelia.




The effects of the LABAs salmeterol and formoterol on the synthesis of soluble interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) in the human airway epithelial cell line A549 was investigated in vitro. Cells cultured for 8 h in the presence of an LABA were stimulated with tumor necrosis factor-alpha for 16 h and then enzyme-linked immunosorbent assays for IL-8, GM-CSF, and VEGF were performed on the supernatants.




Both salmeterol and formoterol significantly suppressed IL-8, GM-CSF, and VEGF secretion from tumor necrosis factor-alpha-stimulated A549 cells. Results indicated that formoterol was more potent than salmeterol in suppressing IL-8 and VEGF production. In contrast, salmeterol appeared to be more potent than formoterol in suppressing GM-CSF production.




LABAs have some anti-inflammatory effects on bronchial epithelia. The differences between salmeterol and formoterol and mechanisms for the observed effects need further evaluation.



Key words:

Adrenergic beta-agonists; Formoterol; Granulocyte-macrophage colony-stimulating factor; Interleukin-8; Salmeterol; Vascular endothelial growth factor A



J Microbiol Immunol Infect. 2007;40:388-394.