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Toxoplasma gondii  ( T. gondii ) can cause zoonotic toxoplasmosis worldwide. Neutrophil extracellular traps (NETs) have been known as a novel effector mechanism against  T. gondii  infection in the innate system of humans, cats, and sheep. Dogs are the intermediate host of  T. gondii , in which the use of NETs against  T. gondii  infection remains unclear. Thus, this study aims to examine the effects of  T. gondii  on NETs release in dogs, and to further investigate the mechanism involved in the process.  T. gondii -triggered NETs were analyzed by scanning electron microscopy (SEM) and fluorescence confocal microscopy, and the mechanism of  T. gondii -triggered NETs release was determined by using inhibitors and a fluorometric reader. The results showed that  T. gondii  tachyzoites significantly triggered NETs-like structures, which consisted of DNA decorated with neutrophil elastase (NE) and myeloperoxidase (MPO). Further investigations revealed that reactive oxygen species (ROS)-, NADPH oxidase-, Rac 1- or p38 mitogen-activated protein kinase (MAPK)-signaling pathways were relevant to  T. gondii  tachyzoites-triggered NETs release. Moreover, zymosan-triggered NETs release was strikingly degraded by  T. gondii  tachyzoites treatment, indicating that  T. gondii  may escape from the NETs-based capture strategy. Taken together, promoting NETs release is suggested to limit motility and evade infection of  T. gondii  in dogs.

Toxoplasma gondii Triggers Neutrophil Extracellular Traps Release in Dogs