Differential transcriptional changes in human alveolar epithelial A549 cells exposed to airborne PM2.5 collected from Shanghai, China

Xiaoning Lei, Joshua E. Muscat, Zhongsi Huang, Chao Chen, Guangli Xiu, Jiahui Chen

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Fine particulate matters (PM2.5) are the core pollutants of haze episode, which pose a serious threat to the human health of developing countries. However, the mechanisms involved in PM2.5-induced hazard influence are not to fully elucidated. In the present study, human lung epithelial cells (A549) were exposed to various concentrations of PM2.5 samples collected from Shanghai, China. Illumina RNA-Seq method with transcriptome, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were further employed to identify the detrimental effects of PM2.5 on A549 cells in vitro. A total of 712 differentially expressed genes were obtained from global transcriptome profiling of A549 cells after PM2.5 exposure. In addition, GO function enrichment analysis revealed that major differentially expressed genes (DEGs) involved in the biological process of the immune system and the response to the stress. KEGG pathway analysis further proposes that infectious disease, cancers, cardiovascular disease, and immune disease pathway were the key human disease events that occur in A549 cells under PM2.5 stress. The data obtained here shed light on the related biological process and gene signaling pathways affected by PM2.5 exposure. This study aids our understanding of the complicated mechanisms related to PM2.5-induced health effects and is informative for the prevention and treatment of PM2.5-induced systemic diseases.

Original languageEnglish (US)
Pages (from-to)33656-33666
Number of pages11
JournalEnvironmental Science and Pollution Research
Volume25
Issue number33
DOIs
StatePublished - Nov 1 2018

All Science Journal Classification (ASJC) codes

  • Environmental Chemistry
  • Pollution
  • Health, Toxicology and Mutagenesis

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