The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites produced by macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2.

In order to investigate the relationship between the activity of alveolar macrophage and the production of PGE2 from activated alveolar macrophage, the authors measured hydrogen peroxide and PGE2 from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica(SiO2) suspended in saline (50 mg/ml) in Sprague-Dawley rats.

1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica. 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05) and PGE2(p>0.05) release from alveolar macrophages. Alveolar macrophages from rats with silicotic nodules released more hydrogen peroxide and PGE2 than those of control group(p<0.05).

These results suggest that silica particle could activate macrophage directly and enhanced the release of PGE2 and hydrogen peroxide from the alveolar macrophage.