Trypanosoma evansi infects a wide range of hosts to cause huge economic losses in livestock industry. In recent years, it has been demonstrated that neutrophils extracellular traps (NETs) play a critical role in combating parasite infections. However, the role of NETs in the resistance to T. evansi infection is still unclear. In this study, T. evansi induced NETs were observed and their components were determined. The effect of NETs on the viability and motility of T. evansi were estimated. The production of reactive oxygen species (ROS) and Lactate dehydrogenase (LDH) activity in the process of T. evansi-induced NETs formation were detected. The effect of ERK1/2 signaling pathway, neutrophil elastase (NE), myeloperoxidase (MPO), store-operated Ca(2+) entry (SOCE) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase on T. evansi triggered NETs formation were determined. The results showed that neutrophils could release ETs after being stimulated with T. evansi and the structures of NETs mainly consisted of DNA decorated with histone 3 (H3), NE, and MPO. NETs could reduce the parasite motility without affecting the parasite viability. T. evansi-induced NETs formation was dose and time-dependent and was accompanied by ROS production. Inhibitor assays suggested that the formation of NETs induced by T. evansi was dependent on MPO, NE and ERK1/2 signaling pathway but independent on NADPH oxidase and SOCE. In addition, there was no significant changes in LDH activity during NETs formation. This study is the first report of T. evansi-induced NETs formation.
Keywords: Extracellular traps; Innate immunity; Neutrophils; Trypanosoma evansi.
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