[Pulmonary fibrosis and inorganic particles]

Abstract

Biological data acquired in recent years has thrown new light on the pathogenesis of pulmonary fibrosis. The key element in the genesis of fibrosis may be the alveolar macrophage which, under the influence of different stimuli, secretes numerous factors, attracting polymorphonuclear leukocytes and eosinophils, stimulating fibroblasts and activating lymphocytes. Pulmonary fibrosis induced by inhalation of inorganic particles seems to proceed by identical mechanisms, with certain differences relating to the nature of each mineral. The morphological, cytological and immunological characteristics which defend the lung from silicosis and asbestosis are particularly discussed. The in vitro reactivity of several cell types (alveolar macrophages, mesothelial cells in culture, fibroblasts) equally has revealed differences between quartz and chrysotile. Nevertheless this in vitro response is difficult to interpret compared to an in vivo response: they vary according to the cellular system used and the physico-chemical state of the particular mineral (chrysotile and leached chrysotile by oxalic acid for example). The fibrosing action of other particles (talc, metals) is also reviewed. As opposed to an inflammatory granuloma secondary to the stimulation of alveolar macrophages which represents the usual response to mineral particles, there is also an immunological granuloma of the sarcoid type which may lead to secondary fibrosis: beryllium and talc in certain circumstances may act by this mechanism.