Silicotic fibrosis: a concept of pulmomonary fibrogenesis

The accumulated evidence indicates that, after ingestion of quartz, macrophages form or release a factor which enables fibroblasts to produce excess hydroxyproline. Inhaled quartz stimulates type II epithelium to generate phospholipid, sometimes in such excess that alveolar lipidosis develops and inhibits fibrosis in rats mainly by isolation of quartz particles from macrophages. Extracted lipid administered parenterally to other rats provokes a marrow monopoiesis, as judged by population kinetics of promonocytes. Prostaglandins, released from stimulated alveolar macrophages, may facilitate monocytic emigration by increasing capillary permeability. Passage of monocytes from pulmonary interstitium to alveolar surface is likely to be simplified by disruption of the thin type I epithelium caused by quartz, a process which the chemotactic action of alveolar lipids could encourage. These interactions are integrated into a system that might be activated by agents other than silica and thus offer a wider concept of pulmonary fibrosis.