Abstract
Neospora caninum causes cattle abortion and neurological symptoms in dogs. Although infection is usually asymptomatic, classical neurological symptoms of neosporosis may be associated with encephalitis. This parasite can grow in brain endothelial cells without markedly damages, but it can modulate the cellular environment to promote its survival in the brain. In previous studies, we described that IFN-γ decreased the parasite proliferation and down regulated nitric oxide (NO) production in astrocyte/microglia cultures. However, it remains unclear how glial cells respond to N. caninum in the presence of neurons. Therefore, we evaluated the effect of 300 IU/mL IFN-γ or 1.0 mg/mL of LPS on infected rat neuron/glial co-cultures. After 72 h of infection, LPS did not affect the mitochondrial dehydrogenase activity. However, IFN-γ decreased this parameter by 15.5 and 12.0% in uninfected and infected cells, respectively. The number of tachyzoites decreased 54.1 and 44.3% in cells stimulated with IFN-γ and LPS, respectively. Infection or LPS treatment did not change NO production. On the other hand, IFN-γ induced increased nitrite release in 55.7%, but the infection reverted this induction. IL-10 levels increased only in infected cultures (treated or not), meanwhile PGE2 release was improved in IFN-γ/infected or LPS/infected cells. Although IFN-γ significantly reduced the neurite length in uninfected cultures (42.64%; p < 0.001), this inflammatory cytokine reverted the impairment of neurite outgrowth induced by the infection (81.39%). The results suggest a neuroprotective potential response of glia to N. caninum infection under IFN-γ stimulus. This observation contributes to understand the immune mediated mechanisms of neosporosis in central nervous system (CNS).
Highlights
Neospora caninum is a protozoan that causes cattle abortion and neurological symptoms in dogs (Wouda et al, 1998; Dubey, 1999; Jolley et al, 1999)
Previous studies of our group described that astrocyte/microglia cultures infected with N. caninum presented a decreased parasite proliferation, release of PGE2 and down modulation of nitric oxide (NO) after IFN-γ stimulation (Jesus et al, 2013)
These events were associated with a parasite escape mechanism and an anti-inflammatory pattern of response by infected glial cells, suggesting a possible glial protective role on nervous tissue during this parasite infection
Summary
Neospora caninum is a protozoan that causes cattle abortion and neurological symptoms in dogs (Wouda et al, 1998; Dubey, 1999; Jolley et al, 1999). Classical neurological symptoms are related with severe multifocal necrotizing encephalitis associated with mononuclear cell infiltration (Malaguti et al, 2012). The blood-brain barrier (BBB) protects the brain against exogenous agents and is constituted by physical, metabolic, and active mechanisms (El-Bachá and Minn, 1999). This parasite overcomes these mechanisms and is able to infect glial cells inducing an immune regulation during protozoan infection in central nervous system (CNS) tissues (Yamane et al, 2000; Pinheiro et al, 2006a,b). Elsheikha et al (2013) showed that N. caninum is able to grow in brain microvascular endothelial cells (fundamental component of the BBB) without markedly disrupting their normal proliferation or mitochondrial integrity and it was associated with an increase in infected cell respiration
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