Fibroblast Proliferation Induced by Silica-exposed Human Alveolar Macrophages

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Abstract
Inhalation of silica dust is an important cause of pulmonary fibrosis. In these studies, we demonstrate that supernatants of silica-stimulated human alveolar macrophages cause significantly (p < 0.05) greater amounts of fibroblast proliferation than do supernatants of macrophages stimulated with optimal amounts of endotoxin (LPS). The amount of fibroblast proliferation was similar (p > 0.2) in the presence of supernatants of LPS-stimulated macrophages and supernatants of unstimulated adherent macrophages. When macrophages were stimulated with LPS in the presence of indomethacin (to inhibit the cyclooxygenase pathway of arachidonic acid), the supernatants stimulated the same amount of proliferation of fibroblasts as did supernatants of silica-stimulated macrophages. Indomethacin did not increase the growth factor activity of supernatants of silica-stimulated or unstimulated macrophages. Consistent with these observations, supernatants of LPS-stimulated macrophages contained 25.5 ± 3.8 nM of PGE2, whereas s...