The cytotoxicity of PM2.5 and its effect on the secretome of normal human bronchial epithelial cells

Exposure to airborne fine particulate matter (PM2.5) induced various adverse health effects, such as metabolic syndrome, systemic inflammation, and respiratory disease. Many works have studied the effects of PM2.5 exposure on cells through intracellular proteomics analyses. However, changes of the extracellular proteome under PM2.5 exposure and its correlation with PM2.5-induced cytotoxicity still remain unclear. Herein, the cytotoxicity of PM2.5 on normal human bronchial epithelia cells (BEAS-2B cells) was evaluated, and the secretome profile of BEAS-2B cells before and after PM2.5 exposure was investigated. A total of 83 proteins (58 upregulated and 25 downregulated) were differentially expressed in extracellular space after PM2.5 treatment. Notably, we found that PM2.5 promoted the release of several pro-apoptotic factors and induced dysregulated secretion of extracellular matrix (ECM) constituents, showing that the abnormal extracellular environment attributed to PM2.5-induced cell damage. This study provided a secretome data for the deep understanding of the molecular mechanism underlying PM2.5-caused human bronchial epithelia cell damage.

Automated summary

This study evaluated the cytotoxicity of PM2.5 on BEAS-2B cells and investigated the changes of extracellular proteome after PM2.5 exposure. PM2.5 was found to promote the release of pro-apoptotic factors and induce dysregulated secretion of extracellular matrix.