The effects of asthma medications on reactive oxygen species production in human monocytes

ABSTRACT

Objective: Asthma is a chronic inflammatory airway disease induced by many environmental factors. The inhalation of allergens and pollutants promotes the production of reactive oxygen species (ROS) leading to airway inflammation, hyper-responsiveness, and remodeling in allergic asthma. The effects of asthma medications on ROS production are unclear. The present study investigated the anti-ROS effects of current asthma medications including inhaled corticosteroid (ICS; budesonide and fluticasone), leukotriene receptor antagonist (LTRA; montelukast), long-acting β2 agonists (LABAs; salmeterol and formoterol), and a new extra-LABA (indacaterol). Methods: The human monocyte cell line THP-1 cells were pre-treated with different concentrations of the asthma medications at different time points after hydrogen peroxide (H₂O₂) stimulation. H₂O₂ production was measured with DCFH-DA by flow cytometry. Results: Montelukast, fluticasone, and salmeterol suppressed H₂O₂-induced ROS production. Indacaterol enhanced H₂O₂-induced ROS production. Budesonide and formoterol alone had no anti-ROS effects, but the combination of these two drugs significantly suppressed H₂O₂-induced ROS production. Conclusions: Different asthma medications have different anti-ROS effects on monocytes. The combination therapy with LABA and ICS seemed not to be the only choice for asthma control. Montelukast may also be a good supplemental treatment for the poorly controlled asthma because of its powerful anti-ROS effects. Our findings provide a novel therapeutic view in asthma.

KEYWORDS:

• Indacaterol
• inhaled corticosteroid (ICS)
• leukotriene receptor antagonist (LTRA)
• long-acting β2 agonist (LABA)
• montelukast

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.

Funding

The study was supported by a grant from Research Center for Environmental Medicine, Kaohsiung Medical University, Taiwan (KMU-TP104A06), National Science Council (NSC 104-2314-B-037-070-MY3 and 103-2314-B-037-013) of the Republic of China, Kaohsiung Medical University Hospital Research Foundation (KMUH102-2T04 and KMUH104-4M58) and grants from Kaohsiung Municipal Hsiao-Kang Hospital (KMHKH-103-013 and KMHKH-104-003).