Toxoplasma gondii induces MLTC-1 apoptosis via ERS pathway.

Toxoplasma gondii (T. gondii) is a serious intracellular parasite and mammalian infection can damage the reproductive system and lead to apoptosis of Murine Leydig tumor cells (MLTC-1); however, the mechanism is unclear. The testis Leydig cell is the main testosterone synthesis cell in male mammals. We studied the mechanism of T. gondii infection on Leydig cell apoptosis in vitro. MLTC-1 were divided into control and experimental groups. Experiment group cells and tachyzoites were co-cultured, in a 1:20 ratio, for 3, 6, 9, and 12 h. T. gondii entered the cells and caused lesions at 12 h. Flow cytometry showed that the apoptosis rate of the experiment group increased with time and was significantly higher (P < 0.05) than the control group. RT-qPCR and western blot demonstrated that the expression of P53, Caspase-3, and Bax were significantly increased at 12 h (P < 0.05). Bcl-2 expression was significantly increased at 12 h (P < 0.05). The ER stress (ERS) pathway was important in cell apoptosis. RT-qPCR and western blot showed that the expression of CHOP was significantly increased at 12 h (P < 0.05). These data indicate that T. gondii induced MLTC-1 cell apoptosis may occur via the ERS pathway.