Polarization of macrophages induced by Toxoplasma gondii and its impact on abnormal pregnancy in rats

Kong, Lanting; Zhang, Qian; Chao, Jing; Wen, Hao; Zhang, Yihua; Chen, He; Pappoe, Faustina; Zhang, Aimei; Xu, Xiaojun; Yue, Cai; Li, Min; Luo, Qingli; Zhang, Linjie; Shen, Jilong

doi:10.1016/j.actatropica.2014.12.001

Cited by 25 publications

(29 citation statements)

References 32 publications

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“…In murine models of adult‐acquired T gondii infection, these classically activated macrophages induced by a Th1 cells contribute to parasite killing . However, the data reported here, in agreement with some previous studies, suggest that these cells are also associated with immunopathology and adverse pregnancy outcomes . Our studies demonstrate that maternal T gondii infection has adverse effects on the maternal‐foetal interface concomitant with inflammation.…”

Section: Discussionsupporting

confidence: 91%

Toxoplasma gondii infection reduces serum progesterone levels and adverse effects at the maternal‐foetal interface

Brito

Silva

Castro

et al. 2019

Parasite Immunology

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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.

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Section: Discussionsupporting

confidence: 91%

Toxoplasma gondii infection reduces serum progesterone levels and adverse effects at the maternal‐foetal interface

Brito

Silva

Castro

et al. 2019

Parasite Immunology

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“…M1 macrophages induced by a Th1 response in murine models exhibit cytotoxic and antimicrobial activities against T. gondii infection. This same response is also associated with immunopathology and adverse pregnancy outcomes . In humans, during implantation, decidual macrophages consist of a M1/M2 heterogeneous activation profile population.…”

Section: Decidual Immune Cells and T Gondii Infectionmentioning

confidence: 97%

How does toxoplasmosis affect the maternal‐foetal immune interface and pregnancy?

Borges

Silva

Brito

et al. 2018

Parasite Immunology

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Toxoplasma gondii is a zoonotic parasite which, depending on the geographical location, can infect between 10% and 90% of humans. Infection during pregnancy may result in congenital toxoplasmosis. The effects on the foetus vary depending on the stage of gestation in which primary maternal infection arises. A large body of research has focused on understanding immune response to toxoplasmosis, although few studies have addressed how it is affected by pregnancy or the pathological consequences of infection at the maternal-foetal interface. There is a lack of knowledge about how maternal immune cells, specifically macrophages, are modulated during infection and the resulting consequences for parasite control and pathology. Herein, we discuss the potential of T. gondii infection to affect the maternal-foetal interface and the potential of pregnancy to disrupt maternal immunity to T. gondii infection. K E Y W O R D Sactivated-macrophage, congenital toxoplasmosis, immunopathogenesis, maternal-foetal Interface, pregnancy, zoonosis

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“…The defensive host reaction against virulent T. gondii involves TNF-α production, and M1 polarization of macrophages, including the induction of the iNOS and IL-6 genes to produce nitric oxide and IL-6, respectively222324. In this study, we reported that the ESAs from the less virulent Chinese 1 TgCtwh3 strain induced lower TNF-α production, and a fewer number of M1 macrophages than the T. gondii Type I RH (Western) strain.…”

mentioning

confidence: 66%

Identification of a TNF-α inducer MIC3 originating from the microneme of non-cystogenic, virulent Toxoplasma gondii

Qiu

Wang

Zhang

et al. 2016

Sci Rep

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Toxoplasma gondii is an opportunistic parasite with avirulent cystogenic and highly virulent non-cystogenic isolates. Although non-cystogenic strains are considered the most virulent, there are also marked genetic and virulence differences among these strains. Excretory-secretory antigens (ESAs) of T. gondii are critical for the invasion process and the immune response of the host. To better understand the differences in virulence between non-cystogenic T. gondii isolates, we studied ESAs of the RH strain (Type I), and the very prevalent in China, but less virulent TgCtwh3 strain (Chinese 1). ESAs of RH and TgCtwh3 triggered different levels of TNF-α production and macrophage M1 polarization. Using iTRAQ analysis, 27 differentially expressed proteins originating from secretory organelles and surface were quantified. Of these proteins, 11 microneme-associated proteins (MICs), 6 rhoptry proteins, 2 dense granule proteins and 5 surface proteins were more abundant in RH than in TgCtwh3. The protein-protein correlation network was employed to identify the important functional node protein MIC3, which was upregulated 5-fold in RH compared with TgCtwh3. MIC3 was experimentally confirmed to evoke a TNF-α secretory response, and it also induced macrophage M1 polarization. This result suggests that MIC3 is a potentially useful immunomodulator that induces TNF-α secretion and macrophage M1 polarization.

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Polarization of macrophages induced by Toxoplasma gondii and its impact on abnormal pregnancy in rats

Cited by 25 publications

References 32 publications

Toxoplasma gondii infection reduces serum progesterone levels and adverse effects at the maternal‐foetal interface

Toxoplasma gondii infection reduces serum progesterone levels and adverse effects at the maternal‐foetal interface

How does toxoplasmosis affect the maternal‐foetal immune interface and pregnancy?

Identification of a TNF-α inducer MIC3 originating from the microneme of non-cystogenic, virulent Toxoplasma gondii

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