Airway inflammation and remodeling in chronic obstructive pulmonary disease: Role of long acting bronchodilators

Yi Han Hsiao, Guang Ming Shiao, Shi Chuan Chang, Diahn Warng Perng

研究成果: Article同行評審

摘要

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and morbidity worldwide. The etiology of COPD is mainly due to chronic exposure of cigarette smoke or air pollutants, causing airway inflammation and remodeling with the consequence of airflow limitation and emphysema. In addition to symptomatic treatment, numerous studies focused on how to inhibit airway inflammation and remodeling of COPD. Anti-inflammatory agents such as corticosteroid, macrolides or phosphodiesterase-4 inhibitor have limitations such as cigarette-smoke related corticosteroid resistance, concerns of major adverse effects, or failure of showing significant anti-remodeling activity. Bronchodilators including long acting muscarinic antagonist, LAMA, and long acting |32-adrenergic receptor agonist, LABA, are mainstay pharmacological choices of COPD. Recent studies have shown that both LAMA and LABA had the abilities to inhibit cigarette smoke-induced airway inflammation and remodeling in vitro and in vivo. However, these anti-inflammatory and anti-remodeling effects remain controversial in the clinical setting. Future studies may be focused on combining different agents, analyzing these effects in different phenotype of COPD patients or larger numbers of study population. (J Intern Med Taiwan 2016; 27: 59-63).

原文English
頁(從 - 到)59-63
頁數5
期刊Journal of Internal Medicine of Taiwan
27
發行號2
出版狀態Published - 4月 2016

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