二氧化硅(SiO_2)所引起的肺纤维化可能与一系列细胞间的互相作用有关,其中包括肺泡巨噬细胞(AM)和肺成纤维细胞(PFB)。PFB的增殖是肺组织对SiO_2刺激的早期反应。以往许多研究曾经证明,用SiO_2染尘的AM释放的白细胞介素I(IL-I)明显高于未染尘者。当大鼠AM与致纤维化的SiO_2培养时,培液中IL-1活力明显升高。本研究用经SiO_2刺激的肺泡巨噬细胞(AM)上清液与肺成纤维细胞(PFB)共培养,在不同时间作观察,发现PFB明显增殖。提示在矽肺纤维化过程中AM、白细胞介素-I(IL-I)和PFB起了关键性作用。 Pulmonary fibrosis induced by silica (SiO 2) may be related to a series of intercellular interactions, including alveolar macrophages (AMs) and pulmonary fibroblasts (PFBs). Proliferation of PFB is an early response of lung tissue to SiO 2 stimulation. Many previous studies have demonstrated that the release of interleukin I (IL-I) by AM-stained AM was significantly higher than that of non-contaminated. IL-1 activity was significantly increased in the culture medium when rat AM and fibrogenic SiO 2 were cultured. In this study, alveolar macrophage (AM) supernatant stimulated with SiO_2 was co-cultured with lung fibroblasts (PFB), observed at different times and found that PFB significantly proliferated. It is suggested that AM, interleukin-1 (IL-I) and PFB play a key role in silicotic fibrosis.