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and IFN-
in Retinal Cell Infection with Toxoplasma gondii1From the Université Paris Descartes, Faculté de Medicine, Hôpital Cochin, Service dophtalmologie, Paris, France; 2Institut Cochin, Département des Maladies Infectieuses, Biologie Comparative des Apicomplexes, Université Paris Descartes, CNRS, (UMR 8104), Paris, France; and 3INSERM U567, Paris, France.
PURPOSE. Toxoplasma gondii is an intracellular protozoan parasite and the most common cause of infectious uveitis. This study was conducted to evaluate the in vitro effect of tumor necrosis factor (TNF)-
and interferon (IFN)-
in rat retinal cells infected with T. gondii.
METHODS. Rat retinal cells, retinal pigment epithelial (RPE) cells, and retinal Müller glial (RMG) cells were in vitro infected with T. gondii RH strain tachyzoites. Cultured cells were stimulated with various concentrations of TNF-
and IFN-
. The effect of TNF-
and IFN-
in T. gondii invasion and replication between retinal cells was determined through two different methods: measuring [3H]-uracil incorporation and counting infected cells by microscopic examination.
RESULTS. Infection by T. gondii was lesser within RPE cells than within RMG cells. IFN-
significantly inhibits [3H]-uracil incorporation in RMG and RPE cells (respectively, 35%, 83%, and 87% inhibition at 0.1, 1, and 10 ng/mL for RMG cells and 0%, 30%, and 75% for RPE cells). TNF-
significantly inhibits [3H]-uracil incorporation in RPE cells (23% and 38% inhibition at 1 and 10 ng/mL), but not in RMG cells. These results were confirmed by confocal microscopic data. The percentage of infected cells decreased from 20% to 7% after IFN-
stimulation.
CONCLUSIONS. Both cytokines IFN-
and TNF-
inhibited T. gondii replication in the RPE cells, whereas only IFN-
had an anti-Toxoplasma activity within the RMG cells. The differences in cytokine response may be the reason that RPE cells are less efficiently infected by T. gondii than are RMG cells.
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