Hillerdal G
Eur J Respir Dis. 1980 Jun;61(3):129-38.
None of the various existing theories on the pathogenesis of pleura plaques (PP) is able to explain their peculiarities. Knowledge of physiology of the lung and pleura and in particular its lymphatic system as well as cellular activities when the cells are exposed to asbestos is necessary when discussing these problems. Short asbestos fibres when phagocytosed by macrophages will activate these cells to produce various substances, among them a factor that will stimulate fibroblasts to produce more collagen. Some of the small fibres will spread towards the visceral pleura of the lung, just like all inhaled dusts. Once in the visceral pleura, some of them will penetrate to the pleural space. There, they will follow the normal lymph flow from the pleural space, which is exclusively through the parietal pleura. Finally, in passing through the parietal pleura, a portion will remain in macrophages there, causing a low-grade stimulation of the submesothelial fibroblasts. After some decades, this will result in visible PP.
关于胸膜斑（PP）发病机制的各种现有理论，均无法解释其独特之处。在讨论这些问题时，有必要了解肺和胸膜的生理学知识，尤其是其淋巴系统，以及细胞接触石棉时的细胞活动。当巨噬细胞吞噬短石棉纤维时，会激活这些细胞产生各种物质，其中一种物质会刺激成纤维细胞产生更多胶原蛋白。一些短纤维会像所有吸入的粉尘一样，向肺的脏层胸膜扩散。一旦进入脏层胸膜，其中一些会穿透到胸膜腔。在那里，它们会随着胸膜腔的正常淋巴液流动，而淋巴液流动仅通过壁层胸膜。最后，在穿过壁层胸膜时，一部分纤维会留在那里的巨噬细胞中，对间皮下单层成纤维细胞产生低度刺激。几十年后，这将导致可见的胸膜斑。
