Lewczuk E, Owczarek H
Kliniki Chorób Wewnetrznych i Zawodowych, Akademii Medycznej we Wrocławiu.
Med Pr. 1994;45(5):441-5.
The damage of pulmonary alveolar epithelial cells occurs in many inflammatory conditions caused by various agents, e.g. asbestos, that involve interstitial lung disease in experimental animals and in humans. After exposure to asbestos alveolar epithelial cells contain significant amount of asbestos fibers and show histologic changes which indicate a marked epithelial injury. The alveolar epithelial injury is manifested by swelling, debris and patchy necrosis of type I cells partly detached from its basement membrane. Besides, regenerative hyperplasia of type II pneumocytes with ultrastructurally cisternal dilation of the rough endoplastic reticulum and significantly greater number of lamellar bodies are found. Following the cessation of exposure, epithelial cells are cleared out of asbestos fibers and return to the normal condition. These data provide insight into pathogenesis of diffuse lung disease and the role of alveolar cells in early and late phases of asbestosis.
肺泡上皮细胞损伤发生在多种由各种因素引起的炎症性疾病中，例如石棉，这在实验动物和人类中都涉及间质性肺病。接触石棉后，肺泡上皮细胞含有大量石棉纤维，并显示出组织学变化，表明存在明显的上皮损伤。肺泡上皮损伤表现为I型细胞肿胀、碎片形成以及部分与其基底膜分离的片状坏死。此外，还发现II型肺细胞再生性增生，其粗面内质网在超微结构上呈池状扩张，板层小体数量显著增加。接触停止后，上皮细胞清除石棉纤维并恢复正常状态。这些数据为深入了解弥漫性肺病的发病机制以及肺泡细胞在石棉肺早期和晚期阶段的作用提供了依据。
