Browsing by Autor "Emmanuel Hermann"

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Congenital Transmission ofTrypanosoma cruziIs Associated with Maternal Enhanced Parasitemia and Decreased Production of Interferon‐γ in Response to Parasite Antigens
(Oxford University Press, 2004) Emmanuel Hermann; Carine Truyens; Cristina Alonso‐Vega; Patricia Rodríguez; Aurélie Berthe; Faustino Torrico; Yves Carlier
The conditions and mechanisms of congenital transmission of Trypanosoma cruzi remain largely unknown. In the present study, we compared the parasitic loads and the immune responses of pregnant T. cruzi-infected women who transmitted parasites to their fetus ("M+B+ mothers") with those of such women who did not transmit parasites to their fetus ("M+B- mothers"). M+B+ mothers had a higher frequency of positive results of hemoculture for T. cruzi than did M+B- mothers, in association with depressed production of parasite-specific interferon- gamma by blood cells that persisted after delivery. In contrast, the production of interleukin (IL)-2, IL-4, and IL-10 and transforming growth factor- beta 1 was similar between both groups of infected mothers, after stimulation with T. cruzi lysate. Flow cytometric analysis showed that T cells and monocytes of M+B+ mothers were less activated than were those of M+B- mothers. Altogether, these results indicate that congenital transmission of T. cruzi is associated with high parasitic loads and peripheral deficient immunological responses in mothers.
Estatus inmunológico de las madres infectadas por T. cruzi.
(Université Libre de Bruxelles, 2005) Cristina Alonso‐Vega; Emmanuel Hermann; Carine Truyens; Patricia Rodríguez; Mary Cruz Torrico; Faustino Torrico; Yves Carlier
The mechanisms of congenital transmission of Chagas disease remain largely unknown. To better understand the role of maternal immunology during pregnancy in congenital Chagas transmission, we studied the cytokine production and the parasitic load in three groups of mothers: infected mothers who transmitted the disease to their babies (M+B+-), infected mothers who did not transmit the disease to their babies (M+B-) and not infected mothers as a control group (M-B-). M+B+ mothers produced less IFNgamma and more IL-10 than the M+B- mothers, and they are not able to produce IL-2. M+B+ mothers showed a higher parasitic load. These results, indicated that the congenital Chagas transmission is associated with an immunological imbalance and a high parasitic load in the M+B+ mothers.
Human Congenital Infection With Trypanosoma cruzi Induces Phenotypic and Functional Modifications of Cord Blood NK Cells
(Springer Nature, 2006) Emmanuel Hermann; Cristina Alonso‐Vega; Aurélie Berthe; Carine Truyens; Amilcar Flores; Marisol Córdova; Lorenzo Moretta; Faustino Torrico; Véronique M. Braud; Yves Carlier
[Immunological status of mothers infected with Trypanosoma cruzi].
(National Institutes of Health, 2005) Cristina Alonso‐Vega; Emmanuel Hermann; Carine Truyens; Patricia Rodríguez; Mary Cruz Torrico; Faustino Torrico; Yves Carlier
The mechanisms of congenital transmission of Chagas disease remain largely unknown. To better understand the role of maternal immunology during pregnancy in congenital Chagas transmission, we studied the cytokine production and the parasitic load in three groups of mothers: infected mothers who transmitted the disease to their babies (M+B+-), infected mothers who did not transmit the disease to their babies (M+B-) and not infected mothers as a control group (M-B-). M+B+ mothers produced less IFNgamma and more IL-10 than the M+B- mothers, and they are not able to produce IL-2. M+B+ mothers showed a higher parasitic load. These results, indicated that the congenital Chagas transmission is associated with an immunological imbalance and a high parasitic load in the M+B+ mothers.
Killer cell immunoglobulin‐like receptor expression induction on neonatal CD8+ T cells in vitro and following congenital infection with Trypanosoma cruzi
(Wiley, 2009) Emmanuel Hermann; Aurélie Berthe; Carine Truyens; Cristina Alonso‐Vega; Rudy Parrado; Faustino Torrico; Yves Carlier; Véronique M. Braud
Major histocompatibility complex (MHC) class I-specific inhibitory natural killer receptors (iNKRs) are expressed by subsets of T cells but the mechanisms inducing their expression are poorly understood, particularly for killer-cell immunoglobulin-like receptors (KIRs). The iNKRs are virtually absent from the surface of cord blood T cells but we found that KIR expression could be induced upon interleukin-2 stimulation in vitro. In addition, KIR expression was enhanced after treatment with 5-aza-2'-deoxycytidine, suggesting a role for DNA methylation. In vivo induction of KIR expression on cord blood T cells was also observed during a human congenital infection with Trypanosoma cruzi which triggers activation of fetal CD8(+) T cells. These KIR(+) T cells had an effector and effector/memory phenotype suggesting that KIR expression was consecutive to the antigenic stimulation; however, KIR was not preferentially found on parasite-specific CD8(+) T cells secreting interferon-gamma upon in vitro restimulation with live T. cruzi. These findings show that KIR expression is likely regulated by epigenetic mechanisms that occur during the maturation process of cord blood T cells. Our data provide a molecular basis for the appearance of KIRs on T cells with age and they have implications for T-cell homeostasis and the regulation of T-cell-mediated immune responses.
Maternal Infection with Trypanosoma cruzi and Congenital Chagas Disease Induce a Trend to a Type 1 Polarization of Infant Immune Responses to Vaccines
(Public Library of Science, 2009) Nicolás Dauby; Cristina Alonso‐Vega; Eduardo Suárez; Amilcar Flores; Emmanuel Hermann; Marisol Córdova; Tatiana Tellez; Faustino Torrico; Carine Truyens; Yves Carlier
These results show that: i) both maternal infection with T. cruzi and congenital Chagas disease do not interfere with responses to BCG, hepatitis B, diphtheria and tetanus vaccines in the neonatal period, and ii) the overcoming of immunological immaturity by T. cruzi infection in early life is not limited to the development of parasite-specific immune responses, but also tends to favour type 1 immune responses to vaccinal antigens.
Monocytes from Uninfected Neonates Born to Trypanosoma cruzi-Infected Mothers Display Upregulated Capacity to Produce TNF-α and to Control Infection in Association with Maternally Transferred Antibodies
(Multidisciplinary Digital Publishing Institute, 2023) Amilcar Flores; Cristina Alonso‐Vega; Emmanuel Hermann; Mary‐Cruz Torrico; Nair Alaide Montaño Villarroel; Faustino Torrico; Yves Carlier; Carine Truyens
Activated monocytes/macrophages that produce inflammatory cytokines and nitric oxide are crucial for controlling Trypanosoma cruzi infection. We previously showed that uninfected newborns from T. cruzi 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. We investigated this possibility by studying the activation status of M+B- cord blood monocytes and their ability to control T. cruzi in vitro infection. We showed that M+B- monocytes have an upregulated capacity to produce the inflammatory cytokine TNF-α and a better ability to control T. cruzi infection than M-B- monocytes. Our study also showed that T. cruzi-specific Abs transferred from the mother play a dual role by favoring trypomastigote entry into M+B- monocytes and inhibiting intracellular amastigote multiplication. These results support the possibility that some M+B- fetuses may eliminate the parasite transmitted in utero from their mothers, thus being uninfected at birth.