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–Regulated Toxoplasma gondii Distribution and Load in the Murine Eye
1From the Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan; and the 2Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
PURPOSE. To establish a mouse model of ocular toxoplasmosis in both wild type (WT) and immunocompromised hosts and to clarify the effects of interferon (IFN)-
on the infectivity of Toxoplasma gondii in various parts of the eye.
METHODS. Susceptible WT C57BL/6, resistant WT BALB/c, and IFN- knockout (GKO) mice were infected with cysts of T. gondii perorally. The tissues were harvested for molecular and histopathologic studies. Analysis included a quantitative competitive polymerase chain reaction (QC-PCR) assay and reverse transcription (RT)-PCR for IFN- and stage conversion markers. All animals underwent ophthalmic examinations including fluorescein angiography (FA).
RESULTS. In WT C57BL/6 mice, T. gondii was detected in tissue in the following order: brain, retina, choroid, sclera, and optic nerve (ON). The highest T. gondii load was observed in the posterior retina, and was much greater than that in WT BALB/c mice. In GKO mice, disseminated infection was evident, and the T. gondii load was highest in the choroid and ON. IFN- mRNA expression in WT C57BL/6 mice was higher than that in WT BALB/c mice after infection. Tachyzoites existed in GKO mice, whereas bradyzoites existed in WT C57BL/6 mice. FA showed dye leakage from the retinal capillaries of GKO mice.
CONCLUSIONS. The T. gondii load in the retina in the susceptible WT strain continued to increase, unlike in the resistant WT strain. IFN- was shown to regulate the T. gondii load and interconversion in the eye. A toxoplasmic vasculitis model was established with GKO mice and assay systems with QC-PCR and FA.
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