scholarly journals Mechanism of Congenital Chagas Disease: Effective Infection Depends on the Interplay Between Trypanosoma cruzi and the Different Tissue Compartments in the Chorionic Villi of the Human Placenta

10.5772/32799 ◽  
2012 ◽  
Author(s):  
Juan Duaso ◽  
Christian Castillo ◽  
Ulrike Kemmerling
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Human Placenta ◽  
Chorionic Villi ◽  
Tissue Compartments

scholarly journals Co-infection with Trypanosoma cruzi (Chagas' disease agent) decreases HIV-1 transcription in human placenta

Retrovirology ◽  
2008 ◽  
Vol 5 (Suppl 1) ◽  
pp. O13
Author(s):  
Guillermina Dolcini ◽  
María Elisa Solana ◽  
Guadalupe Andreani ◽  
Ana María Celentano ◽  
Ana María Donato ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Human Placenta ◽  
Disease Agent ◽  
Hiv 1

scholarly journals Trypanosoma cruzi (Chagas' disease agent) reduces HIV-1 replication in human placenta

Retrovirology ◽  
2008 ◽  
Vol 5 (1) ◽  
pp. 53 ◽  
Author(s):  
Guillermina Laura Dolcini ◽  
Maria Elisa Solana ◽  
Guadalupe Andreani ◽  
Ana Maria Celentano ◽  
Laura Maria Parodi ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Human Placenta ◽  
Disease Agent ◽  
Hiv 1

Trypanosoma cruzi induces tissue disorganization and destruction of chorionic villi in an ex vivo infection model of human placenta

Placenta ◽  
2010 ◽  
Vol 31 (8) ◽  
pp. 705-711 ◽  
Author(s):  
J. Duaso ◽  
G. Rojo ◽  
G. Cabrera ◽  
N. Galanti ◽  
C. Bosco ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Human Placenta ◽  
Ex Vivo ◽  
Infection Model ◽  
Chorionic Villi

The immune response against Trypanosoma cruzi in the human placenta

2017 ◽  
Vol 1 (6) ◽  
pp. 573-577
Author(s):  
Ulrike Kemmerling ◽  
Christian Castillo ◽  
Ana Liempi ◽  
Lisvaneth Medina ◽  
Ileana Carrillo ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Immune Responses ◽  
Chagas Disease ◽  
Defense Mechanisms ◽  
Complex Interaction ◽  
Chorionic Villi ◽  
Congenital Transmission ◽  
Intracellular Parasites ◽  
Chronic Chagas Disease

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.

Dynamics of T Cells Repertoire During Trypanosoma cruzi Infection and its Post-Treatment Modulation

2019 ◽  
Vol 26 (36) ◽  
pp. 6519-6543 ◽  
Author(s):  
Adriana Egui ◽  
Paola Lasso ◽  
Elena Pérez-Antón ◽  
M. Carmen Thomas ◽  
Manuel Carlos López
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Cardiac Tissue ◽  
Acute Infection ◽  
Clinical Status ◽  
Chronic Phase ◽  
Parasite Load ◽  
Chronic Patients ◽  
Cruzi Infection

Chagas disease courses with different clinical phases and has a variable clinical presentation and progression. The acute infection phase mostly exhibits a non-specific symptomatology. In the absence of treatment, the acute phase is followed by a chronic phase, which is initially asymptomatic. This chronic asymptomatic phase of the disease is characterized by a fragile balance between the host’s immune response and the parasite replication. The loss of this balance is crucial for the progression of the sickness. The virulence and tropism of the T. cruzi infecting strain together to the inflammation processes in the cardiac tissue are the main factors for the establishment and severity of the cardiomyopathy. The efficacy of treatment in chronic Chagas disease patients is controversial. However, several studies carried out in chronic patients demonstrated that antiparasitic treatment reduces parasite load in the bloodstream and leads to an improvement in the immune response against the Trypanosoma cruzi parasite. The present review is mainly focused on the cellular patterns associated to the clinical status and the evolution of the disease in chronic patients, as well as the effectiveness of the treatment related to T. cruzi infection control. Therefore, an emphasis is placed on the dynamics of specific-antigens T cell subpopulations, their memory and activation phenotypes, their functionality and their contribution to pathogenesis or disease control, as well as their association with risk of congenital transmission of the parasite.

The Prevalence of Trypanosoma cruzi, the Causal Agent of Chagas Disease, in Texas Rodent Populations

EcoHealth ◽  
2017 ◽  
Vol 14 (1) ◽  
pp. 130-143 ◽  
Author(s):  
Adriana Aleman ◽  
Trina Guerra ◽  
Troy J. Maikis ◽  
Matthew T. Milholland ◽  
Ivan Castro-Arellano ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Causal Agent ◽  
Rodent Populations

scholarly journals Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Marcela Hernández-Torres ◽  
Rogério Silva do Nascimento ◽  
Monica Cardozo Rebouças ◽  
Alexandra Cassado ◽  
Kely Catarine Matteucci ◽  
...  
Keyword(s):  
T Cells ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Parasite Load ◽  
Peritoneal Macrophages ◽  
T Cell Response ◽  
No Production ◽  
Similar Reduction ◽  
Ifn Γ

AbstractChagas disease is a life-threatening disorder caused by the protozoan parasite Trypanosoma cruzi. Parasite-specific antibodies, CD8+ T cells, as well as IFN-γ and nitric oxide (NO) are key elements of the adaptive and innate immunity against the extracellular and intracellular forms of the parasite. Bim is a potent pro-apoptotic member of the Bcl-2 family implicated in different aspects of the immune regulation, such as negative selection of self-reactive thymocytes and elimination of antigen-specific T cells at the end of an immune response. Interestingly, the role of Bim during infections remains largely unidentified. To explore the role of Bim in Chagas disease, we infected WT, Bim+/−, Bim−/− mice with trypomastigotes forms of the Y strain of T. cruzi. Strikingly, our data revealed that Bim−/− mice exhibit a delay in the development of parasitemia followed by a deficiency in the control of parasite load in the bloodstream and a decreased survival compared to WT and Bim+/− mice. At the peak of parasitemia, peritoneal macrophages of Bim−/− mice exhibit decreased NO production, which correlated with a decrease in the pro-inflammatory Small Peritoneal Macrophage (SPM) subset. A similar reduction in NO secretion, as well as in the pro-inflammatory cytokines IFN-γ and IL-6, was also observed in Bim−/− splenocytes. Moreover, an impaired anti-T. cruzi CD8+ T-cell response was found in Bim−/− mice at this time point. Taken together, our results suggest that these alterations may contribute to the establishment of a delayed yet enlarged parasitic load observed at day 9 after infection of Bim−/− mice and place Bim as an important protein in the control of T. cruzi infections.

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