Yu Min, Lou Jianlin, Xia Hailing, Zhang Min, Zhang Yixiao, Chen Junqiang, Zhang Xing, Ying Shibo, Zhu Lijin, Liu Lihong, Jia Guang
Department of Occupational and Environmental Health Science, School of Public Health, Peking University, 38 Xueyuan Road, Beijing, 100191, People's Republic of China.
Department of Occupational Diseases, Zhejiang Academy of Medical Sciences, 182 Tian Mu Shan Road, Zhejiang, 310013, People's Republic of China.
Int Arch Occup Environ Health. 2017 Apr;90(3):265-274. doi: 10.1007/s00420-017-1195-1. Epub 2017 Jan 19.
To examine the effect of asbestos exposure on global DNA methylation and determine whether lung function and inflammatory and fibrosis biomarkers are correlated with the methylation state.
A total of 26 healthy subjects without asbestos exposure (Group 1), 47 healthy subjects with exposure (Group 2), and 52 subjects with benign asbestos-related disorders (ARDs) (Group 3) participated in this cross-sectional study. Blood global 5-methylcytosine (5mC) and serum TNF-α, collagen IV, CCL5 and CC16 concentrations were analyzed using enzyme-linked immunosorbent assay-like assays. Spirometric maneuvers were performed to assess lung function.
Decreased 5mC levels were observed in Groups 2 and 3 compared to Group 1, irrespective of lung function (p < 0.01). There was no significant change in 5mC between Groups 2 and 3. Overall, 5mC was negatively correlated with CCL5 and collagen IV (p < 0.05), but no significant inverse relationship was found between 5mC and CCL5 or collagen IV in each group. Additionally, both 5mC and CC16 were inversely associated with FEV1/FVC% (p = 0.001, adjusted R = 0.145) for non-smokers, and consistently significant inverse relationships were found between CC16 and FEV1/FVC%, independent of asbestos exposure.
Asbestos exposure causes global DNA hypomethylation. DNA hypomethylation has no influence on serum biomarkers and lung function in asbestos-exposed population with or without pleural and pulmonary parenchymal abnormalities.
研究石棉暴露对全基因组DNA甲基化的影响,并确定肺功能、炎症和纤维化生物标志物是否与甲基化状态相关。
共有26名无石棉暴露的健康受试者(第1组)、47名有石棉暴露的健康受试者(第2组)和52名患有良性石棉相关疾病(ARDs)的受试者(第3组)参与了这项横断面研究。使用类似酶联免疫吸附测定的方法分析血液中的全基因组5-甲基胞嘧啶(5mC)以及血清肿瘤坏死因子-α(TNF-α)、IV型胶原、趋化因子配体5(CCL5)和 Clara细胞分泌蛋白16(CC16)的浓度。进行肺量计检查以评估肺功能。
与第1组相比,第2组和第3组的5mC水平降低,与肺功能无关(p < 0.01)。第2组和第3组之间的5mC没有显著变化。总体而言,5mC与CCL5和IV型胶原呈负相关(p < 0.05),但每组中5mC与CCL5或IV型胶原之间未发现显著的负相关关系。此外,对于非吸烟者,5mC和CC16均与第一秒用力呼气容积/用力肺活量百分比(FEV1/FVC%)呈负相关(p = 0.001,调整后的R = 0.145),并且发现CC16与FEV1/FVC%之间始终存在显著的负相关关系,与石棉暴露无关。
石棉暴露导致全基因组DNA低甲基化。DNA低甲基化对有或无胸膜和肺实质异常的石棉暴露人群的血清生物标志物和肺功能没有影响。