High tumor necrosis factor alpha (TNF-alpha) production in Trypanosoma cruzi-infected pregnant mice and increased TNF-alpha gene transcription in their offspring

Rivera, M. T.; Araujo, Sonia; Lucas, Rudolf; Deman, J.; Truyens, Carine; Defresne, Marie-Paule; Baetseĺier, Patrick De; Carlier, Yves

doi:10.1128/iai.63.2.591-595.1995

Cited by 25 publications

(4 citation statements)

References 23 publications

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“…ICAM-1 is induced on target cells by pro-inflammatory cytokines such as IFN-, TNF-, IL-1-and IL-6 (Dustin et al 1986, Rothlein et al 1988, Prieto et al 1992. Sera from mice infected with T. cruzi show higher IFN-, TNFand IL-6 levels (Nabors & Tarleton 1991, Truyens et al 1994, Rivera et al 1995, in parallel with higher amounts of IFN-mRNA in spleens (Nabors & Tarleton 1991). However, cytokine expression during T. cruzi infection has been proven to be organ-specific (Lafaille et al 1990.…”

Section: Discussionmentioning

confidence: 99%

Increased expression and secretion of ICAM‐1 during experimental infection with Trypanosoma cruzi

Laucella¹,

Salcedo

Castaños‐Vélez³

et al. 1996

Parasite Immunology

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In the present study we demonstrate that spleens and hearts from BALB/c mice infected with the virulent Tulahuén or the low virulent CA-I strains of Trypanosoma cruzi, contain substantially higher ICAM-1 transcripts than uninfected controls. ICAM-1 expression in heart cells was also increased in the protein level, as measured by flow cytometry, ELISA and immunohistochemistry. The adhesive receptor was observed not only on inflammatory cells but also on sarcolemma of cardiac myocytes from T. cruzi infected mice. ICAM-1 expression was higher during the acute phase than in the chronic phase of infection, and paralleled the density of inflammatory leukocytes. Elevated titres of soluble ICAM-1 (s-ICAM-1) were detected in sera from mice during the acute phase of infection with CA-I or Tulahuén parasites. Cytokines, including IFN-gamma, IL-1 alpha, IL-6 and TNF-alpha have been shown to modulate expression of ICAM-1. Spleens and hearts from mice infected with CA-I or Tulahuen strains showed increased accumulation of mRNAs specific for these cytokines, which peaked during the acute phase of infection. However, IFN-gamma activity was not necessary for ICAM-1 induction, as its levels were also increased during infection in IFN-gamma receptor knock-out (IFN-gamma R- ) mice. Upregulation of ICAM-1 expression might be a direct consequence of parasite infection, since its density on cell lines of different lineages was enhanced after 24 or 48 h of infection with T. cruzi.

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Section: Discussionmentioning

confidence: 99%

Increased expression and secretion of ICAM‐1 during experimental infection with Trypanosoma cruzi

Laucella¹,

Salcedo

Castaños‐Vélez³

et al. 1996

Parasite Immunology

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“…Chronic maternal infection does not affect reproductive capacity but induces reversible fetal growth retardation (Carlier et al, 1987). Such deleterious effects did not rely on congenital infection but were associated with increased production of TNF-α (Rivera et al, 1995; Mjihdi et al, 2002). In humans, most women of gestational age have a chronic infection (see above).…”

Section: Maternal T Cruzi Systemic Immune Response Gestation and Cmentioning

confidence: 99%

Congenital Transmission of Trypanosoma cruzi: A Review About the Interactions Between the Parasite, the Placenta, the Maternal and the Fetal/Neonatal Immune Responses

et al. 2019

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Chagas disease (CD), caused by the protozoan parasite Trypanosoma cruzi , is considered a neglected tropical disease by the World Health Organization. Congenital transmission of CD is an increasingly relevant public health problem. It progressively becomes the main transmission route over others and can occur in both endemic and non-endemic countries. Though most congenitally infected newborns are asymptomatic at birth, they display higher frequencies of prematurity, low birth weight, and lower Apgar scores compared to uninfected ones, and some suffer from severe symptoms. If not diagnosed and treated, infected newborns are at risk of developing disabling and life-threatening chronic pathologies later in life. The success or failure of congenital transmission depends on interactions between the parasite, the placenta, the mother, and the fetus. We review and discuss here the current knowledge about these parameters, including parasite virulence factors such as exovesicles, placental tropism, potential placental defense mechanisms, the placental transcriptome of infected women, gene polymorphism, and the maternal and fetal/neonatal immune responses, that might modulate the risk of T. cruzi congenital transmission.

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“…Unfortunately, as regards experimental T. cruzi infection, the putative role of TNF-α in thymocyte depletion has not been investigated so far. This topic should be studied, in view of the data showing the enhanced intrathymic contents of this death-related cytokine [ 45 ], and our recent findings that TNF-α is actually involved in the CD8 + T cell apoptosis seen in mesenteric lymph nodes from T. cruzi -infected mice [ 46 ].…”

Section: Introductionmentioning

confidence: 99%

The Thymus Is a Common Target Organ in Infectious Diseases

Savino¹

2006

PLoS Pathog

249

273

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Infectious disease immunology has largely focused on the effector immune response, changes in the blood and peripheral lymphoid organs of infected individuals, and vaccine development. Studies of the thymus in infected individuals have been neglected, although this is progressively changing. The thymus is a primary lymphoid organ, able to generate mature T cells that eventually colonize secondary lymphoid organs, and is therefore essential for peripheral T cell renewal. Recent data show that normal thymocyte development and export can be altered as a result of an infectious disease. One common feature is the severe atrophy of the infected organ, mainly due to the apoptosis-related depletion of immature CD4+CD8+ thymocytes. Additionally, thymocyte proliferation is frequently diminished. The microenvironmental compartment of the thymus is also affected, particularly in acute infectious diseases, with a densification of the epithelial network and an increase in the deposition of extracellular matrix. In the murine model of Chagas disease, intrathymic chemokine production is also enhanced, and thymocytes from Trypanosoma cruzi-infected mice exhibit greater numbers of cell migration-related receptors for chemokines and extracellular matrix, as well as increased migratory responses to the corresponding ligands. This profile is correlated with the appearance of potentially autoreactive thymus-derived immature CD4+CD8+ T cells in peripheral organs of infected animals. A variety of infectious agents—including viruses, protozoa, and fungi—invade the thymus, raising the hypothesis of the generation of central immunological tolerance for at least some of the infectious agent-derived antigens. It seems clear that the thymus is targeted in a variety of infections, and that such targeting may have consequences on the behavior of peripheral T lymphocytes. In this context, thymus-centered immunotherapeutic approaches potentially represent a new tool for the treatment of severe infectious diseases.

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High tumor necrosis factor alpha (TNF-alpha) production in Trypanosoma cruzi-infected pregnant mice and increased TNF-alpha gene transcription in their offspring

Cited by 25 publications

References 23 publications

Increased expression and secretion of ICAM‐1 during experimental infection with Trypanosoma cruzi

Increased expression and secretion of ICAM‐1 during experimental infection with Trypanosoma cruzi

Congenital Transmission of Trypanosoma cruzi: A Review About the Interactions Between the Parasite, the Placenta, the Maternal and the Fetal/Neonatal Immune Responses

The Thymus Is a Common Target Organ in Infectious Diseases

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