Pin I, Godard P
Clinique de Pneumologie, CHU de Grenoble.
Rev Mal Respir. 1994;11(2):111-22.
The mechanisms of airway hyperresponsiveness are numerous and complex. The inflammatory process is one of the most important. It is characterized by epithelial damage and sloughing, by cellular infiltration of the bronchial mucosa and submucosa and by anatomical modifications of the bronchial wall. The cellular infiltrate is characterized by the presence of eosinophils, lymphocytes, monocytes-macrophages and mast cells. These cells are activated and release bronchoconstrictor and proinflammatory mediators. Eosinophils have toxic effects on the bronchial epithelium through the release of basic proteins, while lymphocytes play a central role through the release of cytokines, which can activate and recruit other cells. Mast cells have an important role of starter of the reaction but may also maintain it. Allergen inhalation in the laboratory, when a late response occurs, is responsible for an inflammatory reaction comprising eosinophil influx and activation and T lymphocyte activation. The intensity of the reaction is related to the transient increase in airway hyperresponsiveness confirming the important role of atopy and allergic reactions in airway hyperresponsiveness. However the same kind of inflammatory reaction can be present without atopy and antiinflammatory treatments, even if they reduce airway hyperresponsiveness, may not completely abolish it. This emphasises the complex mechanisms involved in persistent airway hyperresponsiveness.
气道高反应性的机制众多且复杂。炎症过程是其中最重要的机制之一。其特征表现为上皮损伤和脱落、支气管黏膜及黏膜下层的细胞浸润以及支气管壁的结构改变。细胞浸润的特征是存在嗜酸性粒细胞、淋巴细胞、单核细胞 - 巨噬细胞和肥大细胞。这些细胞被激活并释放支气管收缩剂和促炎介质。嗜酸性粒细胞通过释放碱性蛋白对支气管上皮产生毒性作用，而淋巴细胞通过释放细胞因子发挥核心作用，这些细胞因子可激活并募集其他细胞。肥大细胞在反应起始中起重要作用，但也可能维持反应。在实验室中吸入变应原时，若出现迟发反应，则会引发一种炎症反应，包括嗜酸性粒细胞流入和激活以及T淋巴细胞激活。反应强度与气道高反应性的短暂增加有关，这证实了特应性和过敏反应在气道高反应性中的重要作用。然而，即使没有特应性，也可能出现同样类型的炎症反应，而且抗炎治疗虽可降低气道高反应性，但可能无法完全消除它。这凸显了持续性气道高反应性所涉及的复杂机制。
