Girod Carlos E, King Talmadge E
Division of Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9034, USA.
Chest. 2005 Oct;128(4):3055-64. doi: 10.1378/chest.128.4.3055.
Various reports have demonstrated the importance of small airway inflammation in the development of airflow limitation and progression of COPD. This hypothesis proposes that the pathogenesis of COPD mirrors a chronic inhalational dust-induced disease. The putative inorganic dust in cigarette smoke is aluminum silicate or kaolinite, a common component of clay soils. Kaolinite has been recovered in the alveolar macrophages of smokers and has been reported as a constituent of tobacco products. The origin of kaolinite in tobacco products remains unknown, and possible potential sources are proposed. On inhalation, kaolinite deposition in the distal lung may promote macrophage accumulation within the terminal airways leading to a respiratory bronchiolitis. In the susceptible smoker, important genetic, environmental, immunologic, and mechanical factors interact and modulate this small airway inflammation, ultimately leading to the pathologic lesion of emphysema. Further studies into the effects of kaolinite on macrophage function and the subsequent development of respiratory bronchiolitis could lead to prevention of COPD at its precursor lesion.
各种报告已证明小气道炎症在慢性阻塞性肺疾病（COPD）气流受限的发展及病情进展中的重要性。该假说提出，COPD的发病机制反映了一种慢性吸入性粉尘诱发的疾病。香烟烟雾中假定的无机粉尘是硅酸铝或高岭土，这是粘土土壤的常见成分。高岭土已在吸烟者的肺泡巨噬细胞中被发现，并且据报道是烟草制品的一种成分。烟草制品中高岭土的来源尚不清楚，文中提出了可能的潜在来源。吸入时，高岭土在肺远端的沉积可能会促进终末气道内巨噬细胞的积聚，从而导致呼吸性细支气管炎。在易感吸烟者中，重要的遗传、环境、免疫和机械因素相互作用并调节这种小气道炎症，最终导致肺气肿的病理病变。对高岭土对巨噬细胞功能的影响以及随后呼吸性细支气管炎发展的进一步研究，可能会在COPD的前驱病变阶段预防该疾病。
