Abstract
Neospora caninum is an obligate intracellular parasite that causes neurological disorders in dogs and cattle. The majority of host animals are asymptomatic at the chronic stage of infection. However, it remains unclear whether cerebral function is normal in asymptomatic animals. In this study, mice were infected with N. caninum (strain Nc-1) and their brains were examined to understand changes in cerebral function at the chronic stage of infection. Mice infected with N. caninum showed impaired locomotor activity, but no differences in clinical symptoms were observed. In the brains of infected mice, parasites were distributed throughout the brain and histological lesions were observed everywhere except for the cerebellum. Expression levels of proinflammatory cytokines, interferon-gamma and tumour necrosis factor-alpha, were highly upregulated in several brain regions of infected mice. Additionally, the level of neurotransmitters glutamate, glycine, gamma-aminobutyric acid, dopamine and 5-hydroxytryptamine, were altered in infected mice compared with those of uninfected mice. Interestingly, the expression levels of immediately early genes, c-Fos and Arc, in the brain of infected mice were lower than those of in uninfected mice. Our findings may provide insight into neurological disorders associated with N. caninum infection.
Highlights
That N. caninum infection stimulated the immune response in the brain[16], because BALB/c are susceptible to N. caninum and exhibit encephalitis caused by the infection[15]
Because neurological signs appear asymptomatic and become symptomatic, it is important to study the brain of N. caninum-infected asymptomatic animals
Our study is the first to report the behavioral change of mice infected with N. caninum
Summary
That N. caninum infection stimulated the immune response in the brain[16], because BALB/c are susceptible to N. caninum and exhibit encephalitis caused by the infection[15]. Natural hosts chronically infected with N. caninum are usually asymptomatic, the asymptomatic to symptomatic mechanisms of neosporosis onset is still unknown. C57BL/6 male mice are a suitable model for the asymptomatic condition because this strain is relatively resistant to intraperitoneal infection of N. caninum (strain Nc-1). To understand the onset mechanism of neosporosis, we examined sickness behaviour, parasite distribution, histopathological lesions, levels of neurotransmitters (monoamines and amino acids), and expression of IEGs using asymptomatic C57BL/6 male mice during subacute infection with N. caninum. Our findings provide insight into neosporosis associated with brain dysfunction via inflammation, dysregulation of neurotransmitters and downregulation of IEGs
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