Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands.
Pulm Pharmacol Ther. 2011 Aug;24(4):367-72. doi: 10.1016/j.pupt.2011.03.007. Epub 2011 Apr 2.
The pathogenesis of chronic obstructive pulmonary disease (COPD) is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although tobacco smoking is the primary cause of this inhalation injury, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue-repair and -remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The common form of emphysema observed in smokers begins in the respiratory bronchioles near the thickened and narrowed small bronchioles that become the major site of obstruction in COPD. The inflamed airways of COPD patients contain several inflammatory cells including neutrophils, macrophages, T lymphocytes, and dendritic cells. The relative contribution of mast cells to airway injury and remodeling is not well documented. In this review, an overview is given on the possible role of mast cells and their mediators in the pathogenesis of COPD. Activation of mast cells and mast cell signaling in response to exposure to cigarette smoke is further discussed.
慢性阻塞性肺疾病（COPD）的发病机制基于对吸入有毒颗粒和气体的先天和适应性炎症免疫反应。虽然吸烟是这种吸入性损伤的主要原因，但许多其他环境和职业暴露也促成了 COPD 的病理学。与 COPD 相关的免疫炎症变化与组织修复和重塑过程有关，该过程会增加黏液的产生，并导致肺换气表面发生气肿性破坏。在吸烟者中观察到的常见肺气肿形式始于增厚和变窄的小支气管附近的呼吸性细支气管，这些小支气管成为 COPD 中主要的阻塞部位。COPD 患者的炎症气道中含有几种炎症细胞，包括中性粒细胞、巨噬细胞、T 淋巴细胞和树突状细胞。肥大细胞对气道损伤和重塑的相对贡献尚未得到很好的记录。在这篇综述中，概述了肥大细胞及其介质在 COPD 发病机制中的可能作用。进一步讨论了肥大细胞对香烟烟雾暴露的激活和肥大细胞信号转导。
