Tagaya Etsuko, Tamaoki Jun
First Department of Medicine, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Allergol Int. 2007 Dec;56(4):331-40. doi: 10.2332/allergolint.R-07-152. Epub 2007 Nov 1.
Asthma is a chronic inflammatory disease characterized by reversible airflow limitation and airway hyperresponsiveness. Persistent inflammation in airway tissues may lead to structural changes known as airway remodeling and consequently airway obstruction that is not fully reversible and progressive loss of lung function over time. It is generally accepted that airway remodeling is closely related to progression of airway hyperresponsiveness, and the severity of asthma. The structural changes observed in chronic persistent asthma, which includes airway smooth muscle hypertrophy and hyperplasia, collagen deposition to sub-epithelial basement membrane, hyperplasia of goblet cells, thickening of airway mucosa and an increase in vascularity, are derived from airway inflammation. For instance, the thickened airway mucosa might be produced by cytokines and growth factors released from inflammatory cells and airway epithelial cells, and associated with bronchial hyperreactivity and asthma severity. To date, many studies have identified candidate mechanisms and mediators for these observed structural changes, which are thus potential targets in the treatment of asthma. In this review, we describe the recent knowledge of the mechanisms and clinical implications of airway remodeling in asthma.
哮喘是一种慢性炎症性疾病,其特征为可逆性气流受限和气道高反应性。气道组织中的持续性炎症可能导致称为气道重塑的结构变化,并进而导致气道阻塞,这种阻塞不完全可逆,且肺功能会随着时间的推移而逐渐丧失。人们普遍认为,气道重塑与气道高反应性的进展以及哮喘的严重程度密切相关。在慢性持续性哮喘中观察到的结构变化,包括气道平滑肌肥大和增生、上皮下基底膜胶原沉积、杯状细胞增生、气道黏膜增厚和血管增多,均源于气道炎症。例如,增厚的气道黏膜可能由炎症细胞和气道上皮细胞释放的细胞因子和生长因子产生,并与支气管高反应性和哮喘严重程度相关。迄今为止,许多研究已经确定了这些观察到的结构变化的候选机制和介质,因此它们是哮喘治疗中的潜在靶点。在本综述中,我们描述了哮喘气道重塑机制和临床意义的最新知识。