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)-gamma, 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-gamma 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-gamma 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-gamma 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.
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http://dx.doi.org/10.1016/j.parint.2007.01.008 | DOI Listing |
Epigenetics Chromatin
January 2025
Department of Maternal‑Fetal Biology, National Center for Child Health and Development, Tokyo, 157‑8535, Japan.
Background: DNA methylation plays a crucial role in mammalian development. While methylome changes acquired in the parental genomes are believed to be erased by epigenetic reprogramming, accumulating evidence suggests that methylome changes in sperm caused by environmental factors are involved in the disease phenotypes of the offspring. These findings imply that acquired sperm methylome changes are transferred to the embryo after epigenetic reprogramming.
View Article and Find Full Text PDFAJOG Glob Rep
February 2025
Materno-fetal and Obstetrics Research Unit, Department Woman-Mother-Child, Lausanne University Hospital, Lausanne, Switzerland.
J Antimicrob Chemother
January 2025
URP 7328 Federation for Research into Innovative Explorations and Therapeutics in Utero, University of Paris-Cité, Paris, France.
Background: In cases of maternal primary infection with cytomegalovirus (CMV-MPI) maternal treatment with oral valaciclovir 8 g/day has been shown to reduce the risk of fetal infection. The pharmacological profile of this high dosage during pregnancy is not yet known.
Objectives: To quantify maternal-fetal exposure to valaciclovir 8 g/day in a population pharmacokinetic (popPK) study.
Int Immunopharmacol
January 2025
Department of Obstetrics and Gynecology, the First Affiliated Hospital of Anhui Medical University, No 218 Jixi Road, Hefei 230022, Anhui, China; NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract (Anhui Medical University), No 81 Meishan Road, Hefei 230032, Anhui, China; Engineering Research Center of Biopreservation and Artificial Organs, Ministry of Education, No 81 Meishan Road, Hefei 230032, Anhui, China; Innovation Research Institute of Engineering Medicine and Medical Equipment, Anhui Medical University, No 81 Meishan Road, Hefei 230032, Anhui, China; Anhui Provincial Institute of Translational Medicine, No 81 Meishan Road, Hefei 230032, Anhui, China. Electronic address:
Background: The overexpression of HMGB1 at the maternal-fetal interface (MFI) is recognized as a significant factor in Unexplained Recurrent Spontaneous Abortion (URSA). This study aimed to investigate autophagy in the decidual tissues of URSA patients and to explore the relationship between HMGB1 and macrophage autophagy at the MFI in URSA.
Methods: Human decidual tissues were collected from 40 patients diagnosed with URSA and from 60 women undergoing active termination of pregnancy.
J Med Virol
December 2024
Division of Microbiology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
Placental trophoblasts constitute the interface between the fetal and maternal environments and physically prevent maternal-fetal viral transmission. However, congenital human cytomegalovirus (HCMV) infection in the early stages of pregnancy results in severe symptoms in the fetus. HCMV is the most common causative agent of intrauterine infection.
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