Sarir Hadi, Henricks Paul A J, van Houwelingen Anneke H, Nijkamp Frans P, Folkerts Gert
Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, The Netherlands.
Eur J Pharmacol. 2008 May 13;585(2-3):346-53. doi: 10.1016/j.ejphar.2008.03.009. Epub 2008 Mar 18.
Chronic obstructive pulmonary disease (COPD) is a global health problem. Being a progressive disease characterized by inflammation, it deteriorates pulmonary functioning. Research has focused on airway inflammation, oxidative stress, and remodelling of the airways. Macrophages, neutrophils and T cells are thought to be important key players. A number of new research topics received special attention in the last years. The combined use of inhaled corticosteroids and long-acting beta(2)-adrenoceptor agonists produces better control of symptoms and lung function than that of the use of either compound alone. Furthermore, collagen breakdown products might be involved in the recruitment and activation of inflammatory cells by which the process of airway remodelling becomes self-sustaining. Also, TLR (Toll-like receptor)-based signalling pathways seem to be involved in the pathogenesis of COPD. These new findings may lead to new therapeutic strategies to stop the process of inflammation and self-destruction in the airways of COPD patients.
慢性阻塞性肺疾病(COPD)是一个全球性的健康问题。作为一种以炎症为特征的进行性疾病,它会使肺功能恶化。研究主要集中在气道炎症、氧化应激和气道重塑方面。巨噬细胞、中性粒细胞和T细胞被认为是重要的关键因素。在过去几年中,一些新的研究课题受到了特别关注。吸入性糖皮质激素与长效β2肾上腺素受体激动剂联合使用比单独使用任何一种药物能更好地控制症状和肺功能。此外,胶原蛋白分解产物可能参与炎症细胞的募集和激活,通过这一过程气道重塑变得自我维持。另外,基于Toll样受体(TLR)的信号通路似乎也参与了COPD的发病机制。这些新发现可能会带来新的治疗策略,以阻止COPD患者气道中的炎症和自我破坏过程。