Multi-omics analysis to reveal disorders of cell metabolism and integrin signaling pathways induced by PM2.5

Atmospheric fine particle pollution is known to cause many adverse health effects. However, the potential mechanisms of PM2.5-induced cytotoxicity still needs further understanding. Herein, we integrated cytotoxicity, component profiling, metabolomics and proteomics data to deeply explain the biological responses of human bronchial epithelial cells exposed to PM2.5. We observed that PM2.5 caused cell cycle arrest, calcium influx, cell damage and further induced cell apoptosis. The contents of heavy metals and 4-6 rings PAHs in PM2.5 were positively correlated with intracellular ROS, indicating that they might be the important components to induce the above cytotoxicity. Integrated metabolomics and proteomics analysis revealed the significant alterations of many metabolic processes, such as glycolysis, the citric acid cycle, amino acid metabolism and lipid metabolism. Notably, we found that PM2.5 inhibited the integrin signaling pathway, including down-regulating the protein expression of integrins and the phosphorylation of downstream signaling kinases, which might ultimately affect cell cycle progression, cell metabolism and apoptosis. This study provided a comprehensive data resource for the deep understanding of biological toxicity mechanisms caused by atmospheric fine particles in human lungbronchial epithelium cells.

Automated summary

This study integrated cytotoxicity, component profiling, metabolomics, and proteomics data to understand the mechanisms of PM2.5-induced cytotoxicity in human bronchial epithelial cells. PM2.5 was found to cause cell cycle arrest, calcium influx, cell damage, and apoptosis, with heavy metals and PAHs in PM2.5 correlating with intracellular ROS levels. Metabolomics and proteomics analysis revealed significant alterations in metabolic processes, while PM2.5 was shown to inhibit the integrin signaling pathway, affecting cell cycle progression, metabolism, and apoptosis.