Sodium arsenite promotes Pseudomonas aeruginosa-induced apoptosis in human bronchial epithelial cells via H2O2 production.

Exposure to airborne arsenic increases susceptibility to respiratory tract infections caused by pathogenic bacteria, but the exact mechanism is unclear. This study constructed a model of human bronchial epithelial (BEAS-2B) cells exposed to sodium arsenite (NaAsO2). Pseudomonas aeruginosa (PA) was chosen to represent respiratory pathogens. The cells were divided into four groups: the control, the NaAsO2 alone, the PA alone, and the NaAsO2 + PA groups. Cell viability was detected using a CCK-8 assay, apoptosis using flow cytometry and Hoechst staining, and intracellular ROS, H2O2, O2•- and •OH using flow cytometry and the microplate method, respectively. Protein expression was detected by Western blotting. Results showed that treatment with 2.5 μM NaAsO2 for 24 h significantly reduced the cell viability. The release of cellular LDH significantly increased, and the levels of intracellular ROS were markedly elevated. These changes was accompanied by increased apoptosis. The combining NaAsO2 and PA further reduced cell viability and significantly increased the levels of total ROS, O2•-, H2O2, •OH, and the apoptosis rate. Additionally, HO-1 protein levels were lower in BEAS-2B cells treated with both NaAsO2 and PA than in cells treated with NaAsO2 alone. Overall, our results reveal a potential mechanism underlying the combined effects of arsenic and PA exposure on the respiratory tract. These findings provide a theoretical basis for efficiently reducing air pollution-related respiratory diseases.