Autophagy And Silica-Induced Pulmonary Fibrosis

The aim of this study was to investigate the potential role of autophagy in the pathogenesis of pulmonary fibrosis. Pulmonary fibrosis was induced by infusing 1 ml SiO2 (100 mg/ml) suspension to rat trachea. Rats were sacrificed 2, 7, 14, 21, and 28 days after the treatment to detect pulmonary fibrosis and autophagy. Autophagy was assessed by measuring the ratio of LC3II/LC3I, an established marker of autophagy, with Western blot and by detecting autophagic vacuoles with electron microscopy. Pulmonary inflammation and fibrosis were detected with H.E. staining. Pulmonary inflammation was evident early after the exposure to SiO2, which was followed by a marked increase in fibrosis. Compared to the control, LC3II/LC3I ratio and autophagosome in the experimental group were significantly increased 7 days after the treatment, indicating that silica can induce autophagy in the early stage of pneumoconiosis. However, the autophagic indexes were markedly lower in the experimental group than that of the control 14, 21, and 28 days after the treatment, implying that autophagy was suppressed in the late stage of pneumoconiosis. Taken together, these data suggest that autophagy may play different roles in the early and late stages of pneumoconiosis. These findings may provide important new insights into the mechanism underlying the pathogenesis of silica‐induced pulmonary fibrosis.