RESUMEN
Silica particles cause considerable damage to macrophages resulting in their eventual breakdown. At the same time, the development of silicosis involves a number of mechanisms associated with the activation of macrophages. In suggesting schemes for the pathogenesis of this disease many authors associate the central part with activation, completely neglecting damage to cells. Our experiments have shown, however, that much of the activation phenomena could be reproduced in vitro or in vivo by exposing macrophages to macrophage breakdown products. Alternatively, the secondary character of activation is demonstrated by the fact that it reveals itself only at silica doses which cause part of the cells to lose their viability in the same culture. Our data show that the range of macrophage activation phenomena which could be considered as secondary with respect to the breakdown of cells includes the production of neutrophil attractants, enhanced co-operation with T lymphocytes, increase in phagocytic activity, enhancement of cellular O2 consumption and peroxidation, an increase in the activity of dehydrogenases, reduction in the activity of 5'-nucleotidase, and some other effects. Although not denying that small silica doses may be able to exert a direct activating influence upon the macrophage we do, however, believe that the most important and primary role in the pathogenesis of silicosis is played by the damage to and the breakdown of this cell.