Neutrophil extracellular traps (NETs) are released by neutrophils to modulate the immune response. Aluminum (Al) poisoning is linked to immunotoxicity, and selenium (Se) can maintain immune homeostasis. In this study, we investigated the toxic effects of Al on the release of NETs, the antagonistic effect of Se on Al-induced toxicity, and the potential molecular mechanisms underlying these processes. We assessed the cytotoxicity of aluminum on neutrophils using CCK-8 assay, visualized the structure of selenium/aluminum-induced NETs through immunofluorescence and scanning electron microscope, quantified ROS release during NETs formation using fluorescence microplate analysis, and employed the selenoprotein levels to dissect the mechanisms underlying selenium and aluminum-induced NETs release. Peripheral blood neutrophils were exposed to zymosan for a duration of 3 h to induce the formation of NETs. Microscopic analysis indicated that NETs formation was inhibited in the presence of aluminum. Furthermore, assessments using a multifunctional microplate reader demonstrated that aluminum suppressed both the production of extracellular DNA and the reactive oxygen species burst in neutrophils. Western blot analysis revealed that aluminum altered the levels of cellular selenoproteins. In contrast, Se reduced the Al-induced toxic reaction including restored NETs production, ROS burst, and selenoprotein levels. These results indicate that Al decreases the formation of NETs induced by Zym, while Se inhibits the Al toxicity, promoting the formation of NETs by modulating the expression of selenoprotein.
Keywords: Aluminum; Neutrophil extracellular traps; Reactive oxygen species; Selenium; Selenoprotein.
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.