BeWo Trophoblasts are Unable to Control Replication of Toxoplasma gondii, Even in the Presence of Exogenous IFN-γ

Oliveira, J.G.; Silva, N.M.; Santos, Ana Alice D.; Souza, Maria Aparecida de; Ferreira, Gabriela Lícia Santos; Mineo, José Roberto; Ferro, Eloísa Amália Vieira

doi:10.1016/j.placenta.2005.06.006

Cited by 33 publications

(34 citation statements)

References 46 publications

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“…gondii strains may also differ in their ability to survive within the placenta. Replication rates of type I (RH) T. gondii in BeWo choriocarcinoma cells are controversial, with one report asserting slower parasite replication (56) and others reporting normal growth relative to other cell types (5,52). It is unclear, however, how well this cancerous cell line represents primary trophoblasts, as we have shown that BeWo cells do not restrict growth of L. monocytogenes, while primary isolated cytotrophoblasts and explant EVT do (68).…”

Section: Discussionmentioning

confidence: 84%

“…gondii replication. Studies differ on the question of whether T. gondii replication is inhibited in trophoblast cells using the BeWo choriocarcinoma cell line (5,52,56). We have previously shown that L. monocytogenes growth is impaired in EVT (though not BeWo cells) due to altered vacuole maturation (68).…”

Section: Resultsmentioning

confidence: 99%

“…Alternatively, parasites may invade at the decidua-EVT interface, which occupies less than 5% of the maternal-fetal interface (Fig. 1B) (10).Almost all experimental T. gondii infections of the placenta have been performed in mice (6,24,34,54,63), sheep (16), or isolated trophoblast cells (4,7,34,52,55,56). However, none of these models accurately represent the architecture of the human placenta (reviewed in references 43 and 46).…”

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confidence: 99%

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Tissue Barriers of the Human Placenta to Infection with Toxoplasma gondii

et al. 2012

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Toxoplasma gondii is a ubiquitous, obligate intracellular parasite capable of crossing the placenta to cause spontaneous abortion, preterm labor, or significant disease in the surviving neonate. Exploration of the cellular and histological components of the placental barrier is in its infancy, and both how and where T. gondii breaches it are unknown. The human placenta presents two anatomical interfaces between maternal cells and fetal cells (trophoblasts): (i) the villous region where maternal blood bathes syncytialized trophoblasts for nutrient exchange and (ii) the maternal decidua, where mononuclear, extravillous trophoblasts anchor the villous region to the uterus. Using first-trimester human placental explants, we demonstrate that the latter site is significantly more vulnerable to infection, despite presenting a vastly smaller surface. This is consistent with past findings concerning two vertically transmitted viruses and one bacterium. We further explore whether three genetically distinct T. gondii types (I, II, and III) are capable of preferential placental infection and survival in this model. We find no difference in these strains' ability to infect placental explants; however, slightly slower growth is evident in type II (Prugniaud [Pru]) parasites relative to other cell types, although this did not quite achieve statistical significance.T oxoplasma gondii is a ubiquitous parasite of human and veterinary medical importance. This obligate, intracellular protozoan undergoes the sexual portion of its life cycle in cats, the sole definitive host; it also has an asexual life cycle in a broad range of warm-blooded intermediate hosts, most significantly rodents, livestock, and humans. The main modes of transmission are therefore ingestion of oocysts shed in cat feces or of tissue cysts in undercooked meat from intermediate hosts. T. gondii is capable of crossing the blood-brain, blood-ocular, and maternal-fetal barriers. Thus, the vertical route from mother to fetus represents an additional mode of transmission. Fetal infection can cause spontaneous abortion, preterm labor, or significant neurological and ocular sequelae in the surviving offspring.Primary maternal infection during pregnancy is responsible for almost all fetal infection and its frequency depends on human seroprevalence rates that range from ϳ10 to 80% across nations (53). Prenatal testing for toxoplasmosis is routinely offered in many European countries, and drug therapy with spiramycin is prescribed after the diagnosis of maternal infection in order to prevent mother-to-child transmission (19). However, whether prenatal treatment has any effect on vertical transmission is unclear from the results of a systematic review of cohort studies because of numerous biases in the way these studies were designed (65). Randomized controlled clinical trials are needed to obtain evidence for the benefit of prenatal treatment.The mechanisms by which T. gondii infects the placenta and crosses from mother to fetus are poorly understood and experimentally co...

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Section: Discussionmentioning

confidence: 84%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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Tissue Barriers of the Human Placenta to Infection with Toxoplasma gondii

et al. 2012

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“…Barbosa et al [539] showed that in contrast with HeLa cells, treatments with IL-10 or TGF-β1 induced a considerable augmentation in both T. gondii intracellular replication and invasion into BeWo cells. BeWo trophoblasts were unable to control replication of the parasite even in the presence of exogenous IFN-γ [548]. In addition, treatment with IFN-γ alone or associated with IL-10 or TGF-β1 increased the same parameters in BeWo cells, whereas the opposite effect was observed in HeLa cells.…”

Section: T Gondii Infectionmentioning

confidence: 91%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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“…Barbosa et al [599] showed that treatments with IL-10 or TGF-β1 induced a considerable augmentation in both T. gondii intracellular replication and invasion into BeWo trophoblastic cells, in contrast with HeLa cells. BeWo cells were unable to control replication of the parasite even in the presence of exogenous IFN-γ [600] . Nagineni et al [210] reported that in human retinal pigment epithelial cultures TGF-β also enhanced parasite replication.…”

Section: T Gondii Infectionmentioning

confidence: 99%

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

Prandota

2017

Journal of Cardiology and Therapy

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BeWo Trophoblasts are Unable to Control Replication of Toxoplasma gondii, Even in the Presence of Exogenous IFN-γ

Cited by 33 publications

References 46 publications

Tissue Barriers of the Human Placenta to Infection with Toxoplasma gondii

Tissue Barriers of the Human Placenta to Infection with Toxoplasma gondii

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

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