重症哮喘气道重塑机制及治疗研究进展

Research Progress in Mechanism and Treatment of Airway Remodeling in Severe Asthma

气道重塑是重症哮喘重要的病理改变,涉及气道上皮、平滑肌、细胞外基质改变等。慢性炎症是驱动气道重塑的主要因素,气道平滑肌收缩神经调控的改变及负性稳态丢失可能是寡细胞性哮喘中气道重塑与炎症“解偶联”的机制,早期危险因素暴露可通过表观遗传影响气道重塑。高辅助性T细胞(Th细胞)2型炎症是最经典的哮喘内型,也是目前哮喘生物治疗的主要靶点,奥马珠单抗可减轻高分辨率CT上气道壁厚度,但目前关于其他抗体的临床研究较少。重症哮喘中低Th2型炎症比例增加,支气管热成形术可能是有用的策略。抗感染治疗并不能有效逆转气道重塑,气道上皮细胞、平滑肌细胞等结构细胞可能是未来逆转气道重塑的潜在靶点。

Airway remodeling is an important pathological change in severe asthma,involving changes in airway epithelium,smooth muscle,extracellular matrix,etc.Chronic inflammation is the main factor driving airway remodeling.The change of the contractile nerve regulation of airway smooth muscle and the loss of negative homeostasis may be the mechanism of"uncoupling"of airway remodeling and inflammation in oligocellular asthma.Early exposure to risk factors can affect airway remodeling through epigenetics.High helper T cell(Th)2 inflammation is the most classic asthma internal type,and also the main target of asthma biotherapy at present.Omazomab can reduce the thickness of upper airway wall on high-resolution CT,but there are few clinical studies on other antibodies at present.The proportion of low Th2 inflammation in severe asthma is increasing,and bronchial thermoplasty may be a useful strategy.Anti-infection therapy cannot effectively reverse airway remodeling,and airway epithelial cells,smooth muscle cells and other structural cells may be potential targets for reversing airway remodeling in the future.