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Toxoplasma gondii infection reduces serum progesterone levels and adverse effects at the maternal‐foetal interface
Author(s) -
Brito Carina,
M. Silva Tânia,
M. Castro Maria,
Wyrwas Weronika,
Oliveira Bárbara,
M. Fonseca Bruno,
Oliveira Pedro,
W. Roberts Craig,
Teixeira Natércia,
Borges Margarida
Publication year - 2020
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12690
Subject(s) - toxoplasma gondii , biology , pregnancy , immunology , immune system , spleen , immunity , fetus , placenta , toxoplasmosis , antibody , genetics
Aims Pregnant BALB/c mice infected with a Toxoplasma gondii type II strain were used to determine how pregnancy interferes with the development of maternal immunity to T gondii and how infection disrupts pregnancy and foetal development. Methods Maternal and foetal parasite loads were assessed by amplification of T gondii SAG1 using qPCR. Adverse effects of infection were evaluated on foetal‐placental development by quantification of implantation units undergoing resorption and by histopathological analyses. Serum progesterone levels were quantified by immunoassay. The effect of T gondii infection on maternal immunity was determined by assessing the cellular composition of spleens by flow cytometry. Results Infected pregnant mice exhibited clinical signs of infection, inflammation and necrosis at the maternal‐foetal interface and decreased serum progesterone levels. In infected mice, there was a clear effect of pregnancy and infection on macrophage cell numbers. However, no differences in the parasite load were detected between non‐pregnant and pregnant mice. Conclusions Maternal T gondii infection induced adverse effects at the maternal‐foetal interface. Alterations were found in immune spleen cells, dependent on the day of pregnancy, relative to nonpregnant animals. The results obtained suggest a pregnancy‐dependent mechanism during T gondii infection able to interfere with macrophage numbers.