Oliver Brian G, Black Judith L
School of Medical Sciences Pharmacology, University of Sydney, NSW, Australia.
Allergol Int. 2006 Sep;55(3):215-23. doi: 10.2332/allergolint.55.215.
The airway smooth muscle is the key determinant of airway narrowing in asthma but its function in the absence of disease is unknown. Evidence for an intrinsic abnormality in the muscle in asthma is only just emerging. The airway smooth muscle is not merely a contractile cell, but also one which determines the composition of, and interacts with the extracellular matrix, and which may participate in inflammatory and allergic reactions and viral infections. The reason for the differences which have been observed in the in vitro properties of airway smooth muscle derived from asthmatic individuals may result from an inherent "supercontractility", an increased tendency to proliferate due to the absence of an inhibitory transcription factor C/EBP-alpha, the influence of an altered extracellular matrix and/or a decrease in release of factors such as PGE(2) which would under normal circumstances inhibit both proliferation and contraction. Although long acting beta agonists and corticosteroids are successful treatments for inflammation and bronchoconstriction, the structural changes which constitute airway remodelling may require additional therapeutic intervention, the nature of which will be determined by thorough investigation of the mechanisms underlying the asthmatic phenotype.
气道平滑肌是哮喘中气道狭窄的关键决定因素，但其在无疾病状态下的功能尚不清楚。哮喘中肌肉内在异常的证据才刚刚出现。气道平滑肌不仅是一种收缩细胞，而且还决定细胞外基质的组成并与之相互作用，并且可能参与炎症、过敏反应和病毒感染。从哮喘患者中获取的气道平滑肌体外特性所观察到的差异，其原因可能是内在的“超收缩性”、由于缺乏抑制性转录因子C/EBP-α而导致的增殖倾向增加、细胞外基质改变的影响和/或诸如PGE(2)等因子释放减少（在正常情况下PGE(2)会抑制增殖和收缩）。尽管长效β受体激动剂和皮质类固醇是治疗炎症和支气管收缩的成功药物，但构成气道重塑的结构变化可能需要额外的治疗干预，其性质将通过对哮喘表型潜在机制的深入研究来确定。
