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

2019 ◽  
Vol 10 ◽  
Author(s):  
Ulrike Kemmerling ◽  
Antonio Osuna ◽  
Alejandro Gabriel Schijman ◽  
Carine Truyens
2017 ◽  
Vol 1 (6) ◽  
pp. 573-577
Author(s):  
Ulrike Kemmerling ◽  
Christian Castillo ◽  
Ana Liempi ◽  
Lisvaneth Medina ◽  
Ileana Carrillo ◽  
...  

Congenital Chagas disease, caused by Trypanosoma cruzi (T. cruzi), is partially responsible for the increasing globalization of Chagas disease despite its low transmission. During congenital transmission, the parasite reaches the fetus by crossing the placental barrier. However, the success or impairment of congenital transmission of the parasite is the product of a complex interaction between the parasite, the maternal and fetus/newborn immune responses and placental factors. There is other evidence apart from the low congenital transmission rates, which suggests the presence of defense mechanisms against T. cruzi. Thus, the typical amastigote nests (intracellular parasites) cannot be observed in placentas from mothers with chronic Chagas disease nor in human placental chorionic villi explants infected in vitro with the parasite. In the latter, only a few parasite antigens and DNA are identified. Accordingly, other infections of the placenta are not commonly observed. All these evidences suggest that the placenta can mount defense mechanisms against T. cruzi.


2014 ◽  
Vol 109 (8) ◽  
pp. 1005-1013 ◽  
Author(s):  
Ana Luiza Cassin Duz ◽  
Paula Melo de Abreu Vieira ◽  
Bruno Mendes Roatt ◽  
Rodrigo Dian Oliveira Aguiar-Soares ◽  
Jamille Mirelle de Oliveira Cardoso ◽  
...  

2010 ◽  
Vol 124 (2) ◽  
pp. 219-224 ◽  
Author(s):  
Leony Cristina Caetano ◽  
José Clóvis do Prado ◽  
Miriam Paula Alonso Toldo ◽  
Ana Amélia Carraro Abrahão

2009 ◽  
Vol 42 (5) ◽  
pp. 484-487 ◽  
Author(s):  
Sergio Sosa-Estani ◽  
Estela Cura ◽  
Elsa Velazquez ◽  
Cristina Yampotis ◽  
Elsa Leonor Segura

The objective was to detect Trypanosoma cruzi infection in 32 children in Salta, Argentina, born to 16 chronically infected young women who were treated with benznidazole. Tests were performed to assess the efficacy of treatment after 14 years. At the end of the follow up, 87.5% of the women were non-reactive to EIA tests, 62.5% to IHA and 43.8% to IFA. 62.5% of the women were non-reactive according to two or three serological tests. No infected children were detected among the newborns of mothers treated before their pregnancy.


2016 ◽  
Vol 127 ◽  
pp. 80S
Author(s):  
Bruna Belo ◽  
Analice Prata ◽  
Adriana Moura ◽  
Leandro Nobrega ◽  
Melania M. Amorim ◽  
...  

2010 ◽  
Vol 105 (5) ◽  
pp. 687-691 ◽  
Author(s):  
Christopher S Eickhoff ◽  
Olivia K Giddings ◽  
Nobuko Yoshida ◽  
Daniel F Hoft

2003 ◽  
Vol 71 (6) ◽  
pp. 3165-3171 ◽  
Author(s):  
Vladimir Michailowsky ◽  
Keith Luhrs ◽  
Manoel Otávio C. Rocha ◽  
David Fouts ◽  
Ricardo T. Gazzinelli ◽  
...  

ABSTRACT Sera and peripheral blood mononuclear cells (PBMC) from patients displaying different clinical symptoms as well as from normal uninfected individuals (NI) were used to evaluate the humoral and cellular responses of Chagas' disease patients to Trypanosoma cruzi-derived paraflagellar rod proteins (PFR). Our results show that sera from both asymptomatic Chagas' disease patients (ACP) and cardiac Chagas' disease patients (CCP) have higher levels of antibodies to PFR than sera from NI. Immunoglobulin G1 (IgG1) and IgG3 were the main Ig isotypes that recognized PFR. We also tested three recombinant forms of PFR, named rPAR-1, rPAR-2, and rPAR-3, by Western blot analysis. Sera from seven out of eight patients with Chagas' disease recognized one of the three rPAR forms. Sera from 75, 50, and 37.5% of Chagas' disease patients tested recognized rPAR-3, rPAR-2, and rPAR-1, respectively. PFR induced proliferation of 100 and 70% of PBMC from ACP and CCP, respectively. Further, stimulation of cells from Chagas' disease patients with PFR enhanced the frequencies of both small and large CD4+ CD25+ and CD4+ CD69+ lymphocytes, as well as that of small CD8+ CD25+ lymphocytes. Finally, we evaluated the ability of PFR to elicit the production of gamma interferon (IFN-γ) by PBMC from patients with Chagas' disease. Fifty percent of the PBMC from ACP as well as CCP produced IFN-γ upon stimulation with PFR. PFR enhanced the percentages of IFN-γ-producing cells in both CD3+ and CD3− populations. Within the T-cell population, large CD4+ T lymphocytes were the main source of IFN-γ.


Sign in / Sign up

Export Citation Format

Share Document