Respiratory exposure is the major route of atmospheric PM2.5 entering the human body.Epidemiological studies have indicated that exposure to PM2.5 is associated with increased pulmonary diseases risk but the underlying mechanisms remain less clear.In this study,human bronchial epithelial cells(BEAS-2B)were used to investigate the toxic effect and biological mechanism of PM2.5 collected from Beijing,China,based on microarray analysis and following bioinformatics analysis.Result of microarray analysis manifested that PM2.5 affected the expression of 1636 genes,including 867 genes that were up-regulated and 769 genes that were down-regulated.These differentially expressed genes were then subjected to bioinformatics analysis,in order to explore the biological process changes induced by PM2.5 in BEAS-2B cells.Gene ontology(GO)analysis indicated that PM2.5 caused significant changes in gene expression patterns related to a series of important functions,covering gene transcription,signal transduction,cell proliferation,cellular metabolic processes,immune response,etc.Additionally,pathway analysis and signal-net analysis showed that PI3K/Akt,MAPK,and TNF signaling pathway as well as Pathways in cancer were the most prominent significant pathways affected by PM2.5,which played key regulatory role in cell proliferation,cell differentiation,cytoskeleton regulation,and inflammatory.Finally,for the purpose of verifing the accuracy of microarray analysis,qRT-PCR was introduced to dectect the expression of part key genes in the above signaling pathways,which were selected from the signal-net.Our study provided a large amount of information for the molecular mechanism underling PM2.5 caused pulmonary diseases,and follow-up researches are still needed for further exploit.