Experimental Silicosis: A Model for the Study of Inflammatory Pulmonary Reticulin

Abstract

In rats rendered silicotic by an intratracheal injection of silica, early silicotic nodules were found to undergo regressive changes. These regressive changes were recognized predominantly by degenerative changes in the reticulin of intra-alveolar tissue. The degenerating intra-alveolar tissue was very similar to that seen in so-called “organizing” pneumonia. Some of the degenerative changes in pulmonary inflammatory reticulin occurred spontaneously in immature, apparently “normal” silicotic nodules. They also occurred in animals injected intratracheally with enzymes as well as with pooled human sera. Severe destructive changes in reticulin were also frequently observed in regions of bronchopneumonia. The spontaneous degeneration of intra-alveolar reticulin suggests that some immature silicotic nodules may never mature and may disintegrate. The destruction of immature silicotic nodules in regions of bronchopneumonia may result in a more widespread intrapulmonary dissemination of liberated quartz dust on the one hand, and on the other hand, in a loss of some of the quartz dust by pulmonary clearance. If it were possible to induce regressive changes in the reticulin of silicotic tissue with exogenous agents, without endangering the life of the animal, such treatment may have important application to some chronic pulmonary diseases where inflammatory reticulin is the predominant stromal component. The data obtained in this study do not prove that intratracheal injections of enzyme or serum affected inflammatory reticulin tissue though a suggestion of such occurrence exists.