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BACKGROUND: The neonatal receptor for the constant fraction (Fc) of IgG (FcRn), expressed in syncytiotrophoblast and endothelial cells of the fetal vessels of the placenta, has the function of transferring maternal IgG in order to provide immunity to the fetus. Despite its protective role, various infectious agents use this mechanism to cross the placenta and infect the product. During T. gondii infection, specific IgG antibodies are produced that coat the parasite, facilitating its transplacental passage. OBJECTIVE: To determine the association between infection with IgG-coated T. gondii, FcRn expression and placental alterations in mice in the last third of gestation. MATERIAL AND METHODS: BALB/c mice were used, inoculated with 5 million parasites (ME49 strain) on day 15 of gestation, through the coccygeal vein, with: 1) PBS; 2) uncoated tachyzoites and 3) IgG-coated tachyzoites. Three days post-infection, the placentas of one uterine horn were processed for histopathology and immunohistochemistry to detect FcRn and T. gondii. In the other horn, the levels of the receptor mRNA (RT-qPCR) and the presence of parasite DNA (qPCR) were determined. RESULTS AND DISCUSSION: Toxoplasma gondii infection caused placental insufficiency due to vascular changes (thrombosis, hemorrhage and congestion), with more severe alterations in the group inoculated with IgG-coated tachyzoites and with a greater number of fetuses that presented growth restriction. Placentas with uncoated parasites showed lower expression of FcRn at the protein level, not mRNA, which is contrary to what was expected. IgG-coating was related to an increase or decrease in FcRn expression in different placental areas. CONCLUSIONS: Infection with Toxoplasma gondii and its IgG-coating modifies the expression of FcRn in the placenta and induces greater placental damage, which induces fetal growth restriction. [ABSTRACT FROM AUTHOR]

The SARS-COV 2 virus has led to a rapidly transmitting pandemic with a high death rate. There is a subregistry of confirmed cases due to the wide spectrum of clinical manifestations and the possibility of dissemination through asymptomatic patients. Studies are still lacking to confirm whether there is vertical transmission, however, the newborn may be infected through the placenta, direct contact with the mother or during hospital stay, so protective measures must be taken during maternal, perinatal and neonatal care. [ABSTRACT FROM AUTHOR]