Systemic and placental productions of tumor necrosis factor contribute to induce fetal mortality in mice acutely infected with Trypanosoma cruzi

Mjihdi, Abdelkarim; Truyens, Carine; Detournay, Olivier; Carlier, Yves

doi:10.1016/j.exppara.2004.03.016

Cited by 16 publications

(10 citation statements)

References 35 publications

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“…For example, overproduction of IFNG and TNFA is associated with preterm labor and recurrent spontaneous abortions in humans as well as fetal rejection in mice [7, 8, 50]. On the other hand, the same cytokines may also control trophoblast invasion in early pregnancy and play a role in parturition at term [9, 10, 51–54].…”

Section: Discussionmentioning

confidence: 99%

Expression and Function of PDCD1 at the Human Maternal-Fetal Interface1

Taglauer

Trikhacheva

Slusser

et al. 2008

Biology of Reproduction

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The failure to reject the semiallogenic fetus by maternal T lymphocytes suggests that potent mechanisms regulate these cells. PDCD1 is a CD28 family receptor expressed by T cells, and its ligand CD274 is strongly expressed by trophoblast cells of the human placenta. In this study, we examined whether human maternal T cells express PDCD1. Immunofluorescence examination of uterine tissues revealed PDCD1 expression on CD3+ cells was low in nonpregnant endometrium but increased in first-trimester decidua and remained elevated in term decidua (P < 0.05). In addition, higher relative proportions of term decidual CD8bright, CD4+, and regulatory T cells expressed PDCD1 in comparison to autologous peripheral blood (P < 0.05). Term decidual T cells also expressed full-length and soluble PDCD1 mRNA isoforms more abundantly than their peripheral blood counterparts (P ≤ 0.05). We also examined the effects of PDCD1:CD274 interactions in decidual T cells. Jar choriocarcinoma cells were transfected with CD274 and cocultured with activated decidual CD4+ or CD8bright T cells for 72 h followed by analysis of cytokine concentration and decidual T cell apoptosis. Compared with empty vector-transfected cells, CD274-transfected Jar cells caused a significant suppression of interferon gamma and tumor necrosis factor alpha production by CD4+ (P < 0.05) but not CD8bright T cells, while having no effect on secretion of IL10 or T cell apoptosis. These results suggest that the PDCD1:CD274 pathway functions in modification of maternal decidual lymphocyte cytokine secretion during pregnancy.

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Section: Discussionmentioning

confidence: 99%

Expression and Function of PDCD1 at the Human Maternal-Fetal Interface1

Taglauer

Trikhacheva

Slusser

et al. 2008

Biology of Reproduction

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“…Neonatal morbidity and mortality are much higher when acute or reactivated infection (co-infection with HIV) occur during pregnancy (see Section 4; Freilij et al, 1995b;Moretti et al, 2005;Scapellato et al, 2009), as well as, likely, when chronically infected pregnant women suffer from re-infections (see Section 9; Torrico et al, 2006). Experiments in mice also show acute infection and reinfections in chronic phase inducing fetal resorptions and/or pup mortality (Mjihdi et al, 2002;Solana et al, 2002;Cencig et al, 2013; see Section 9), in relation to high blood parasite-and TNF-␣-levels (Mjihdi et al, 2002(Mjihdi et al, , 2004Solana et al, 2009). (1) Reactivated Chagas disease: data according to Scapellato et al, 2009; (2) acute Chagas disease: data according to Bittencourt (1992) and Moretti et al, 2005; (3) chronic Chagas disease: average transmission rates in endemic and non endemic countries (EC and NEC, respectively) according to Howard et al (2014).…”

Section: T Cruzi Infection and Pregnancy Outcomesmentioning

confidence: 92%

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

2015

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The aim of this paper is to discuss the main ecological interactions between the parasite Trypanosoma cruzi and its hosts, the mother and the fetus, leading to the transmission and development of congenital Chagas disease. One or several infecting strains of T. cruzi (with specific features) interact with: (i) the immune system of a pregnant woman whom responses depend on genetic and environmental factors, (ii) the placenta harboring its own defenses, and, finally, (iii) the fetal immune system displaying responses also susceptible to be modulated by maternal and environmental factors, as well as his own genetic background which is different from her mother. The severity of congenital Chagas disease depends on the magnitude of such final responses. The paper is mainly based on human data, but integrates also complementary observations obtained in experimental infections. It also focuses on important gaps in our knowledge of this congenital infection, such as the role of parasite diversity vs host genetic factors, as well as that of the maternal and placental microbiomes and the microbiome acquisition by infant in the control of infection. Investigations on these topics are needed in order to improve the programs aiming to diagnose, manage and control congenital Chagas disease.

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“…For example, Porphyromonas gingivalis infection in mice augmented maternal TNF-␣ production while suppressing maternal IL-10, leading to increased fetal resorptions (25). Trypanosoma cruzi infection in mice induced high levels of maternal TNF-␣, resulting in increased fetal mortality (28). The placental Th1 response against Leishmania infection resulted in increased fetal resorptions in infected mice (20).…”

Section: Vol 78 2010mentioning

confidence: 99%

Salmonella entericaSerovar Typhimurium-Induced Placental Inflammation and Not Bacterial Burden Correlates with Pathology and Fatal Maternal Disease

et al. 2010

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Food-borne infections caused by Salmonella enterica species are increasing globally, and pregnancy poses a high risk. Pregnant mice rapidly succumb to S. enterica serovar Typhimurium infection. To determine the mechanisms involved, we addressed the role of inflammation and bacterial burden in causing placental and systemic disease. In vitro, choriocarcinoma cells were a highly conducive niche for intracellular S. Typhimurium proliferation. While infection of mice with S. Typhimurium wild-type (WT) and mutant (⌬aroA and ⌬invA) strains led to profound pathogen proliferation and massive burden within placental cells, only the virulent WT S. Typhimurium infection evoked total fetal loss and adverse host outcome. This correlated with substantial placental expression of granulocyte colony-stimulating factor (G-CSF), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-␣) and increased serum inflammatory cytokines/chemokines, such as G-CSF, IL-6, CCL1, and KC, evoked by WT S. Typhimurium infection. In contrast, infection with high doses of S. Typhimurium ⌬aroA, despite causing massive placental infection, resulted in reduced inflammatory cellular and cytokine response. While S. Typhimurium WT bacteria were dispersed in large numbers across all regions of the placenta, including the deeper labyrinth trophoblast, S. Typhimurium ⌬aroA bacteria localized primarily to the decidua. This correlated with the widespread placental necrosis accompanied by neutrophil infiltration evoked by the S. Typhimurium WT bacteria. Thus, the ability of Salmonella to localize to deeper layers of the placenta and the nature of inflammation triggered by the pathogen, rather than bacterial burden, profoundly influenced placental integrity and host survival.Typhoid fever in humans, caused by Salmonella enterica serovar Typhi, is widespread in developing nations with poor hygienic conditions, whereas nontyphoidal intestinal disease caused by S. enterica serovar Typhimurium, a food-borne pathogen, is of global concern (17). Vaccines against typhoid fever offer variable protection against different serovars and have had limited use (24). Salmonella species are also becoming more resistant to antibiotics (19). Young, elderly, pregnant, and HIV-infected individuals form the high-risk groups for Salmonella infections (7). The mouse model of S. Typhimurium infection mimics human typhoid, causing disseminated disease. The T-cell response to S. Typhimurium is generally detectable only beyond 7 to 14 days (26, 37). Thus, innate immunity and inflammatory cytokines are critical in controlling the early primary infection (47).Salmonella species can cause pregnancy complications such as chorioamnionitis, transplacental fetal infection, abortions, and neonatal and maternal septicemia (15,44). Intracellular infections in general can lead to pregnancy complications such as preterm labor and preeclampsia (12,29,38). Infections with many chronic intracellular pathogens may also be exacerbated during pregnancy and/or pose a risk of reactivation postpartum (3,2...

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Systemic and placental productions of tumor necrosis factor contribute to induce fetal mortality in mice acutely infected with Trypanosoma cruzi

Cited by 16 publications

References 35 publications

Expression and Function of PDCD1 at the Human Maternal-Fetal Interface1

Expression and Function of PDCD1 at the Human Maternal-Fetal Interface1

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

Salmonella entericaSerovar Typhimurium-Induced Placental Inflammation and Not Bacterial Burden Correlates with Pathology and Fatal Maternal Disease

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