Busse W W, Calhoun W F, Sedgwick J D
Department of Medicine, University of Wisconsin, Madison 53792.
Am Rev Respir Dis. 1993 Jun;147(6 Pt 2):S20-4. doi: 10.1164/ajrccm/147.6_Pt_2.S20.
Airway inflammation has emerged as an important contributor to mechanisms of asthma. Furthermore, the presence of airway inflammation is present even in the absence of severe symptoms. To study the mechanisms by which bronchial inflammation can occur in asthma, a number of models have been developed including the airway response to antigen in allergic subjects. The pattern that has emerged from such studies indicates prompt pulmonary mast-cell activation and the apparent initiation of an inflammatory response. This inflammatory response develops over hours and is important in the later and more persistent development of bronchial obstruction. The eosinophil is an important cell in this process as are proinflammatory cytokines generated from activated lung mononuclear cells. The consequence of this multiple cell, multiple proinflammatory product interaction is the establishment of a self-perpetuating, redundant process by which asthma severity increases.
气道炎症已成为哮喘发病机制的一个重要因素。此外，即使在没有严重症状的情况下，气道炎症也依然存在。为了研究哮喘中支气管炎症发生的机制，人们开发了许多模型，包括过敏受试者对抗原的气道反应。这些研究得出的模式表明，肺部肥大细胞迅速激活，炎症反应明显启动。这种炎症反应在数小时内发展，对支气管阻塞的后期和更持续发展很重要。嗜酸性粒细胞在这个过程中是一种重要的细胞，活化的肺单核细胞产生的促炎细胞因子也是如此。这种多细胞、多种促炎产物相互作用的结果是建立了一个自我持续、多余的过程，哮喘严重程度因此增加。
