RESUMO
Neutrophils represent an important part of the body's innate immunity and can resist the invasion of pathogenic microorganisms by releasing neutrophil extracellular traps (NETs). In this study, we investigated the toxic effects of lead (Pb) on the release of NETs, the antagonism of selenium (Se) on Pb toxicity and the potential molecular mechanisms. Our model was an in vitro exposure model for the addition of Se, Pb or both in the culture medium and was based on the separation of neutrophils from the peripheral blood of healthy chickens. Phorbol-myristate-acetate (PMA) was used as a stimulant. The scanning electron microscopy and fluorescence microscopy results showed that Pb weakened the PMA-induced formation of NETs. Exposure to Pb reduced the expression of the extracellular regulated protein kinase (ERK) pathway and the respiratory burst. Exposure to Pb also attenuated the release of Ca2+ in the endoplasmic reticulum mediated by the inositol 1,4,5-trisphosphate receptor (IP3R). These are two ways by which Pb decreases the formation of NETs. Pb also attenuates the expression levels of myeloperoxidase (MPO) and neutrophil elastase (NE), and attenuates histone removal by affecting the expression of different protein kinase C (PKC) isoforms. In contrast, Se can reduce the toxic damage caused by Pb. These results indicate that exposure to Pb decreases the formation of NETs, while Se can antagonize the toxicity of Pb to allow the formation of NETs.