The formation of canine neutrophil extracellular traps induced by sodium arsenic in polymorphonuclear neutrophils.

As a novel defense effector mechanism of host innate immune system, neutrophil extracellular traps (NETs) plays an important role against pathogens infection and several diseases. In this study, we investigated the influence of sodium arsenic on novel effector mechanism of NETs generated by polymorphonuclear neutrophils (PMN) and the potential molecular mechanism. Sodium arsenic-induced NETs formation was observed by fluorescence confocal microscopy. Quantitation of NETs induced by sodium arsenic was determined by fluorescence microplate. In parallel experiments, inhibitors of ERK1/2-, p38 MAPK - signaling pathways were used. The results showed that sodium arsenic significantly induced formation of NETs-like structures in PMNs, and these extracellular thicker and thinner networks were mainly composed by DNA decorated with histones, neutrophils elastase (NE) and myeloperoxydase (MPO), which suggests main classical characteristics of NETs induced by sodium arsenic. Furthermore, arsenic markedly increased quantitation of NETs, which further confirmed that sodium arsenic indeed triggered NETs release. However, inhibition of NADPH oxidase, ERK1/2- and p38 MAPK-signaling pathways did not change sodium arsenic-induced NETs formation, suggesting sodium arsenic-induced NETs was a NADPH oxidase, ERK1/2-, p38 MAPK -signaling pathways-independent process. Even though more potential molecular mechanisms involved in sodium arsenic-induced NETs formation call for investigation, our study is the first to report the novel function of PMNs-NETs formation induced by sodium arsenic, which might provide an entirely new view of perceiving and understanding the role of sodium arsenic in therapeutic implications in clinics and overexposure diseases.