稀土钕尘肺工人血清中IL-10、IFN-γ的表达及其DNA甲基化分析

Expression of IL-10 and IFN-gamma in Serum of Neodymium Pneumoconiosis and DNA Methylation Analysis

尘肺病是由于长期吸入粉尘颗粒物并沉积于肺部,引起以肺纤维病变为主的疾病。在此过程中,DNA甲基化可以调节细胞因子基因活性,影响Th1、Th2型细胞因子的转录,导致Th1/Th2细胞因子之间失衡,可能是导致尘肺形成的重要原因。为明确尘肺与DNA甲基化的关系,本研究检测了尘肺病人和健康人群的全血钕含量、血清中Th1型细胞因子IFN-γ、Th2型细胞因子IL-10的表达和IFN-γ、IL-10基因启动子区甲基化状态,了解了稀土钕尘肺工人钕暴露水平和机体免疫状况,初步探讨DNA甲基化在钕粉尘致肺纤维化中的作用。结果表明,氧化钕体内高蓄积、IL-10与IFN-γ基因启动子区的甲基化水平改变,导致IL-10表达升高、IFN-γ表达降低,在钕尘肺的病情进展中起重要作用。

Pneumoconiosis is a disease of pulmonary fibrosis caused by long-term inhalation of dust particles and deposition in the lungs.DNA methylation can regulate the activity of cytokine genes,affect the transcription of Th1 and Th2 cytokines and lead to the imbalance between Th1 and Th2 cytokines,which may be an important cause of pneumoconiosis formation.To clarify the relationship between pneumoconiosis and DNA methylation,we tested the whole blood neodymium content,the expression of Th1 cytokines IFN-γ、Th2 cytokines in serum and the methylation status of promoter region of IFN-γ、IL-10 gene in pneumoconiosis patients and healthy population,studied the level of neodymium exposure and immune status of workers with rare earth neodymium pneumoconiosis,and mainly discussed the role of DNA methylation in pulmonary fibrosis induced by neodymium dust.The results showed that the high accumulation of neodymium oxide in vivo,the change of methylation level of IL-10 and IFN-γgene promoter region resulted in the increase of IL-10 expression and the decrease of IFN-γexpression,which played an important role in the progress of neodymium pneumoconiosis.