目的:应用甲基化芯片与生物信息技术，筛选大气污染细颗粒物（PMn 2.5）对人支气管上皮（HBE）细胞的差异甲基化位点及其包含的基因和通路，为进一步研究PMn 2.5对HBE细胞毒理学机制提供科学依据。n 方法:于2020年8月，用10 μg/ml和50 μg/ml PMn 2.5水溶物染毒HBE细胞24 h，即PMn 2.5 10 μg/ml染毒组（低剂量组）和PMn 2.5 50 μg/ml染毒组（高剂量组）；用未染毒的HBE细胞作为对照组，将DNA片段与芯片进行杂交，芯片扫描读取数据后分析数据，筛选差异甲基化位点，进行差异甲基化位点的GO分析和KEGG分析，功能表观遗传模块（FEMs）分析整体差异甲基化位点的相互作用关系。n 结果:与对照组比较，低剂量组共筛选出127个差异甲基化位点，包含89个基因，其中甲基化水平升高的有55个位点，甲基化水平降低的有72个，甲基化差异位点主要集中在Body区域和UTR区域。与对照组比较，高剂量组共筛选出238个差异甲基化位点，包含168个的基因，其中甲基化水平升高的有127个位点，甲基化水平降低的有111个，其差异位点也主要集中在Body区域和UTR区域。通过FEMs分析，筛选出8个相互作用最多的基因，其中6个基因有明显甲基化水平变化。在低剂量组的甲基化差异位点中找到与细胞凋亡相关的n MALT1基因；在高剂量组的甲基化差异位点中找到与癌变相关的n PIK3CA、n ARID1A基因；在FEMs分析结果中找到与肿瘤抑制相关的n TNF基因。n 结论:PMn 2.5染毒HBE细胞后，引起DNA甲基化水平明显变化，筛选出细胞凋亡和癌变相关基因，提示PMn 2.5致癌致突变作用可能与DNA甲基化有关。n “,”Objective:To screen the differential methylation sites, genes and pathways of air pollution fine particles (PMn 2.5) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PMn 2.5 on HBE cells.n Methods:In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM n 2.5 aqueous solution for 24 h, namely PMn 2.5 10 μg/ml exposure group (low dose group) and PM n 2.5 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs).n Results:Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. n MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; n PIK3CA and n ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; n TNF genes related to tumor inhibition were found in the results of FEMs analysis.n Conclusion:After PMn 2.5 exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PMn 2.5 may be related to DNA methylation.n