Monocytes from Uninfected Neonates Born to -Infected Mothers Display Upregulated Capacity to Produce TNF-α and to Control Infection in Association with Maternally Transferred Antibodies.

Activated monocytes/macrophages that produce inflammatory cytokines and nitric oxide are crucial for controlling infection. We previously showed that uninfected newborns from infected mothers (M+B- newborns) were sensitized to produce higher levels of inflammatory cytokines than newborns from uninfected mothers (M-B- newborns), suggesting that their monocytes were more activated. Thus, we wondered whether these cells might help limit congenital infection.

The macrophage infectivity potentiator of induces innate IFN-γ and TNF-α production by human neonatal and adult blood cells through TLR2/1 and TLR4.

We previously identified the recombinant (r) macrophage (M) infectivity (I) potentiator (P) of the protozoan parasite (Tc) (rTcMIP) as an immuno-stimulatory protein that induces the release of IFN-γ, CCL2 and CCL3 by human cord blood cells. These cytokines and chemokines are important to direct a type 1 adaptive immune response. rTcMIP also increased the Ab response and favored the production of the Th1-related isotype IgG2a in mouse models of neonatal vaccination, indicating that rTcMIP could be used as a vaccine adjuvant to enhance T and B cell responses.

Macrophage-infectivity potentiator of (TcMIP) is a new pro-type 1 immuno-stimulating protein for neonatal human cells and vaccines in mice.

This work identifies the protein "macrophage infectivity potentiator" of trypomastigotes, as supporting a new property, namely a pro-type 1 immunostimulatory activity on neonatal cells. In its recombinant form (rTcMIP), this protein triggers the secretion of the chemokines CCL2 and CCL3 by human umbilical cord blood cells from healthy newborns, after 24h culture. Further stimulation for 72h results in secretion of IFN-γ, provided cultures are supplemented with IL-2 and IL-18.

Epigenetic signature of exposure to maternal infection in cord blood cells from uninfected newborns.

To assess the epigenetic effects of exposure to maternal infection. We performed an epigenome-wide association study to compare the DNA methylation patterns of umbilical cord blood cells from uninfected babies from chagasic and uninfected mothers. DNA methylation was measured using Infinium EPIC arrays.

Mitigation of benznidazole toxicity and oxidative stress following ascorbic acid supplementation in an adult traveller with chronic indeterminate Chagas' disease.

Background: Benznidazole is an effective drug in the trypanocidal treatment of acute and chronic indeterminate Chagas' disease (CD). However, adverse drug reactions (ADR) are common and frequently cause patients to discontinue treatment.

Objectives: We hypothesized that antioxidant supplementation could mitigate benznidazole-induced toxicity.

Is Antibody-Dependent Enhancement of Infection Contributing to Congenital/Neonatal Chagas Disease?

The newborns of women infected with the parasite (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route).

Geographic Variations in Test Reactivity for the Serological Diagnosis of Trypanosoma cruzi Infection.

Chagas disease is a neglected disease caused by Trypanosoma cruzi parasites. Most diagnosis is based on serological tests, but the lack of a gold standard test complicates the measurement of test performance. To overcome this limitation, we used samples from a cohort of well-characterized T.

Helminth infection induces non-functional sensitization to house dust mites.

Background: IgE characterizes the humoral response of allergic sensitization but less is known about what modulates its function and why some patients present clinical symptoms for a given IgE level and others do not. An IgE response also occurs during helminth diseases, independently of allergic symptoms. This response could be a model of non-functional IgE.

Hookworm treatment induces a decrease of suppressive regulatory T cell associated with a Th2 inflammatory response.

Background: Like other helminths, hookworms (HW) induce a regulatory immune response able to modulate and dampen reactivity of the host to antigens. No data about the evolution of the immune response after treatment are available. We aim to phenotype the regulatory immune response during natural HW infection and its evolution after treatment.

Lipoteichoic acid stimulates the proliferation, migration and cytokine production of adult dental pulp stem cells without affecting osteogenic differentiation.

Aim: To model in vitro the contact between adult dental pulp stem cells (DPSCs) and lipoteichoic acid (LTA), a cell wall component expressed at the surface of most Gram-positive bacteria.

Methodology: Human DPSCs obtained from impacted third molars were cultured and exposed to various concentrations of S. aureus LTA (0.

-associated myocarditis mimicking acute myocardial infarction.

Background: Trichinellosis is a parasitic infection caused by nematodes of the genus , and its principal mode of transmission is the consumption of raw or undercooked contaminated meat. Cardiac involvement in trichinellosis is unusual, yet it represents the most frequent cause of death. Here, we report a case in which -associated myocarditis simulated a myocardial infarction.

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

Chagas disease (CD), caused by the protozoan parasite , 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.

Phylogenetic Analysis of Trypanosoma cruzi from Pregnant Women and Newborns from Argentina, Honduras, and Mexico Suggests an Association of Parasite Haplotypes with Congenital Transmission of the Parasite.

Trypanosoma cruzi, the causative agent of Chagas disease, exhibits a high genetic variability and has been classified into six discrete typing units (DTUs) named TcI through TcVI. This genetic diversity is believed to be associated with clinical characteristics and outcomes, but evidence supporting such associations has been limited. Herein, we performed a phylogenetic analysis of T.

Comparison of methodologies for detecting Trypanosoma cruzi parasites by microscopic observation of microhematocrit capillary tubes.

Introduction: The microscopic examination of microhematocrit tubes (mHCT) has been proposed as the gold standard for acute and congenital Chagas disease diagnosis. We compared different mHCT methodologies detecting T. cruzi parasites in the blood.

Congenital Transmission of in Argentina, Honduras, and Mexico: An Observational Prospective Study.

Compared with South America, there is a lack of epidemiologic studies about the risk of congenital transmission of in Central America and Mexico. It has been suggested that genotypes might differ by region and that congenital transmission might vary according to the parasite's genotype. Our objective was to compare congenital transmission rates in three countries.

Infection Favors Elimination IL-12/IFNγ-Dependent Pathways.

This study develops an original co-infection model in mice using , the most frequent cause of human brucellosis, and , the agent of African trypanosomiasis. Although the immunosuppressive effects of in natural hosts and mice models are well established, we observed that the injection of in mice chronically infected with induces a drastic reduction in the number of in the spleen, the main reservoir of the infection. Similar results are obtained with - and -infected mice and -infected mice co-infected with , demonstrating that this phenomenon is not due to antigenic cross-reactivity.

The Ly49E Receptor Inhibits the Immune Control of Acute Infection.

The protozoan parasite circulates in the blood upon infection and invades various cells. Parasites intensively multiply during the acute phase of infection and persist lifelong at low levels in tissues and blood during the chronic phase. Natural killer (NK) and NKT cells play an important role in the immune control of infection, mainly by releasing the cytokine IFN-γ that activates the microbicidal action of macrophages and other cells and shapes a protective type 1 immune response.

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

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.

Congenital transmission of Trypanosoma cruzi in Argentina, Honduras, and Mexico: study protocol.

Background: Trypanosoma cruzi has been divided into Discrete Typing Units I and non-I (II-VI). T. cruzi I is predominant in Mexico and Central America, while non-I is predominant in most of South America, including Argentina.

Differential IFN-γ production by adult and neonatal blood CD56+ natural killer (NK) and NK-like-T cells in response to Trypanosoma cruzi and IL-15.

Early interferon-gamma (IFN-γ) release by innate cells is critical to direct type 1 immune response able to control intracellular pathogens like Trypanosoma cruzi. Although CD56(bright) natural killer (NK) cells are reported to be potent early IFN-γ producers, other CD56(+) cells like CD56(dim) NK cells and NK-like T cells have recently been shown to also release IFN-γ. We have here studied the contribution of each CD56(+) lymphocyte populations in early IFN-γ production in both adults and neonates.

Monocytes play an IL-12-dependent crucial role in driving cord blood NK cells to produce IFN-g in response to Trypanosoma cruzi.

We previously reported that foetuses congenitally infected with Trypanosoma cruzi, the agent of Chagas disease, mount an adult-like parasite-specific CD8(+) T-cell response, producing IFN-g, and present an altered NK cell phenotype, possibly reflecting a post-activation state supported by the ability of the parasite to trigger IFN-g synthesis by NK cells in vitro. We here extended our knowledge on NK cell activation by the parasite. We compared the ability of T.

Fertility, gestation outcome and parasite congenital transmissibility in mice infected with TcI, TcII and TcVI genotypes of Trypanosoma cruzi.

This work aims to compare the effects of acute or chronic infections with the T. cruzi genotypes TcI (X10 strain), TcII (Y strain) and TcVI (Tulahuen strain) on fertility, gestation, pup growth and the possible vertical transmission of parasites in BALB/c mice. The occurrence of congenital infection was evaluated by microscopic examination of blood and/or qPCR on blood and heart in newborn pups and/or older offspring submitted to cyclophosphamide-induced immunosuppression in order to detect possible cryptic congenital infection.