Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice

Toxoplasma gondii infection is generally asymptomatic in immunocompetent persons but can be life-threatening in immunocompromised persons and for fetuses in the case of maternal–fetal transmission. The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity against T. gondii infection, on maternal–fetal transmission of T. gondii was analyzed by quantitative competitive polymerase chain reaction targeting T. gondii-specific SAG1 gene. T. gondii loads were obvious in uterus and placenta of wild type (WT) C57BL/6 (B6, susceptible strain) but not BALB/c (resistant strain) pregnant mice. Higher levels of T. gondii were detected in uterus and placenta of IFN-γ knock-out (GKO) B6 and BALB/c than in those of WT mice. Furthermore, T. gondii was detected in fetus of GKO B6 but not GKO BALB/c, WT B6, or WT BALB/c mice. Thus, not only IFN-γ but also genetic susceptibility to T. gondii infection was important for the protective immunity of maternal–fetal transmission of T. gondii to fetus via placenta. T. gondii-infected WT mice displayed a low delivery rate with high IFN-γ production, whereas infected GKO mice did not. Additionally, mean body weight of neonates from T. gondii-infected GKO BALB/c pregnant mice was significantly lower than that of unaborted neonates from WT BALB/c pregnant mice, suggesting the effects of T. gondii infection on intrauterine growth retardation of fetus in pregnant GKO mice.