First description of enhanced expression of glia maturation factor-beta in experimental toxoplasmic encephalitis

OBJECTIVE: We previously showed that Toxoplasma gondii infection induces severe neuropathology in the form of oxidative stress, high nitric oxide production, glial activation, and apoptosis. This study examined the association between glia maturation factor-beta (GMF-β) expression, activated astrocytes/microglia, and neuropathology in toxoplasmic encephalitis (TE). METHODS: Mouse brain GMF expression was examined by immunohistochemistry on days 10 and 30 post-T. gondii infection. RESULTS: Neuropathology of infected mice was associated with increased GMF expression in reactive glial cells and neurons compared with healthy controls. Specific up-regulation of GMF-β expression in glial cells was associated with increased gliosis in TE. CONCLUSIONS: GMF up-regulation in glial cells causes neuronal destruction, suggesting a TE pathological pathway involving GMF-mediated brain cell cytotoxicity. GMF-β may therefore be a good biomarker for disease risk assessment and to estimate host neuropathy after exposure to T. gondii, as well as providing a new therapeutic target. This is the first study to demonstrate the expression of GMF-β in reactive glial cells and its association with neuropathology in TE.