摘要
暴露于煤尘会导致煤工尘肺病(CWP)的发展,这是一种与下呼吸道巨噬细胞积累有关的疾病。控制单核细胞招募的机制仍然知之甚少。由于单核细胞趋化蛋白-1 (MCP-1)被认为是血液单核细胞的一种有效趋化因子,我们分析了CWP患者肺间室中MCP-1的存在。分析了16名非吸烟对照者和27名非吸烟CWP患者(16名单纯性尘肺(SP)和11名进行性大规模纤维化(PMF))的支气管肺泡灌洗液(BALF)。粘附法纯化肺泡巨噬细胞(AMs),冻干法浓缩BALF 10倍。使用夹芯酶联免疫吸附试验(ELISA)在BALF和3h上清液中测定MCP-1。通过免疫组化方法对3例CWP患者和2例对照组的组织切片进行肺组织中MCP-1的定位。SP或PMF患者的高浓度BALF中MCP-1水平显著高于对照组(中位11 pg x mL-1)(分别为370和555 pg x mL-1) (p<0.001)。CWP患者的AM上清液中MCP-1的释放增强(中位83 pg x mL-1),但与对照组(中位41 pg x mL-1)相比,该水平没有达到显著性。尽管CWP患者BALF中AM计数显著增加,但与MCP-1水平无关。 MCP-1 levels in BALF correlated with MCP-1 levels in AM supernatants (p=0.47; p<0.02). In control lung specimens, MCP-1 was expressed by a few AMs, type II pneumocytes and perivascular smooth muscle cells. CWP sections were characterized by an increased number of AMs and mainly by the presence of fibroblasts (in the myogenic area of fibrotic lesions) and hyperplastic type II pneumocytes, which were strongly immunostained for MCP-1. Our data demonstrate that: 1) patients with coal worker's pneumoconiosis have a marked pulmonary overproduction of monocyte chemoattractant protein-1; and 2) in addition to alveolar macrophages, fibroblasts (probably myofibroblasts) and hyperplastic type II pneumocytes may also be responsible for this increased level of monocyte chemoattractant protein-1 in coal worker's pneumoconiosis.