Toxoplasma gondii can cause parasitic encephalitis, a life-threatening infection predominately occurs in immunocompromised individuals. T. gondii has the ability to invade the brain, but the mechanisms by which this parasite crosses the blood-brain-barrier (BBB) to cause brain damage remain incompletely understood. The present study reports the structural and functional changes associated with infection and replication of T. gondii within human cerebrovascular endothelial cells (ECs) in vitro. Our results indicated that exposure of ECs to T. gondii had adverse impact on the function and integrity of the ECs - through reduced viability and increased monolayer permeability as well as altered expression of cytokine and tight junction genes. The P-glycoprotein (P-gp) inhibitor verapamil was found to be effective in inhibiting T. gondii crossing the ECs in a dose-dependent manner. The present study showed that T. gondii can compromise several functions of human cerebrovascular endothelial cells and demonstrated the ability of verapamil to inhibit T. gondii crossing of the BBB-ECs in vitro.
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