Abstract
Background: anticholinergics are commonly used for the treatment of COPD. They exert their bronchodilatory effect by blocking the muscarinic receptors in the lungs. Animal studies demonstrated a pro-inflammatory role of muscarinic m3 receptors in airway inflammation, however little is known about the role of anticholinergics in innate immunity.
Aim: investigating the role of anticholinergics in innate immunity in COPD bronchial epithelial cells with special emphasis on the impact on antiviral immune response.
Method: epithelial cells obtained from bronchial brushings from COPD patients were expanded by in vitro culture. Cells were pre-treated with ipratropium, tiotropium or budesonide, alone or in combinations, in different concentrations for 18h followed by stimulation with a TLR-3 agonist (PIC)and compound for 3 or 24h. Expression of TLR3 and different cytokines is determined at gene level by RT-qPCR.
Results: PIC induced TSLP expression at 3h, which was decreased by budesonide. Expression of TLR3 at 24h did not change upon treatment with any of the drugs. IFN-beta expression is induced at 3h and was not decreased by anticholinergics, but by budesonide. Expression of IL-8 is induced at 3h and to a greater extent at 24h and was not altered by treatment with anticholinergics. TNF-alpha expression at 3h and 24h remained sustained and did not change upon treatment with any of the drugs. IL-32 expression at 24h was not decreased by any of the drugs.
Conclusion: our preliminary data show no inhibitory effects of anticholinergics on antiviral response in COPD epithelial cells whereas glucocorticosteroid treatment reduced IFN-beta gene expression.
- Copyright ©ERS 2015
