Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections

Chagas disease is caused by Trypanosoma cruzi infection. Besides the host-related factors, such as immune response and genetic background, the parasite, strain, and occurrences of reinfection episodes, may influence disease outcome. Our results demonstrate that both the primary infection and the rei...

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Main Authors: Juliana Reis Machado, Marcos Vinícius Silva, Diego Costa Borges, Crislaine Aparecida da Silva, Luis Eduardo Ramirez, Marlene Antônia dos Reis, Lúcio Roberto Castellano, Virmondes Rodrigues, Denise Bertulucci Rocha Rodrigues
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2014/648715
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spelling doaj-2baa6e5b6b7c4b45a51ba93965d15f632020-11-25T00:52:20ZengHindawi LimitedBioMed Research International2314-61332314-61412014-01-01201410.1155/2014/648715648715Immunopathological Aspects of Experimental Trypanosoma cruzi ReinfectionsJuliana Reis Machado0Marcos Vinícius Silva1Diego Costa Borges2Crislaine Aparecida da Silva3Luis Eduardo Ramirez4Marlene Antônia dos Reis5Lúcio Roberto Castellano6Virmondes Rodrigues7Denise Bertulucci Rocha Rodrigues8Laboratory of Immunology, Federal University of Triângulo Mineiro, Cefores, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilLaboratory of Immunology, Federal University of Triângulo Mineiro, Cefores, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilDiscipline of Cell Biology, Federal University of Triângulo Mineiro, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilLaboratory of Immunology, Federal University of Triângulo Mineiro, Cefores, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilDiscipline of Parasitology, Federal University of Triângulo Mineiro, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilDiscipline of Pathology, Federal University of Triângulo Mineiro, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilTechnical School of Health, Federal University of Paraíba, 58051-900 João Pessoa, PB, BrazilLaboratory of Immunology, Federal University of Triângulo Mineiro, Cefores, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilLaboratory of Immunology, Federal University of Triângulo Mineiro, Cefores, Frei Paulino Street, 30, 38025-180 Uberaba, MG, BrazilChagas disease is caused by Trypanosoma cruzi infection. Besides the host-related factors, such as immune response and genetic background, the parasite, strain, and occurrences of reinfection episodes, may influence disease outcome. Our results demonstrate that both the primary infection and the reinfection with the Colombiana strain are connected with lower survival rate of the mice. After reinfection, parasitaemia is approximately ten times lower than in primary infected animals. Only Colombiana, Colombiana/Colombiana, and Y/Colombiana groups presented amastigote nests in cardiac tissue. Moreover, the mice infected and/or reinfected with the Colombiana strain had more T. cruzi nests, more intense inflammatory infiltrate, and higher in situ expression of TNF-α and IFN-γ than Y strain. Antigen-stimulated spleen cells from infected and/or reinfected animals produced higher levels of TNF-α, IFN-γ, and IL-10. Our results reinforce the idea that Chagas disease outcome is influenced by the strain of the infective parasite, being differentially modulated during reinfection episodes. It highlights the need of control strategies involving parasite strain characterization in endemic areas for Chagas disease.http://dx.doi.org/10.1155/2014/648715
collection DOAJ
language English
format Article
sources DOAJ
author Juliana Reis Machado
Marcos Vinícius Silva
Diego Costa Borges
Crislaine Aparecida da Silva
Luis Eduardo Ramirez
Marlene Antônia dos Reis
Lúcio Roberto Castellano
Virmondes Rodrigues
Denise Bertulucci Rocha Rodrigues
spellingShingle Juliana Reis Machado
Marcos Vinícius Silva
Diego Costa Borges
Crislaine Aparecida da Silva
Luis Eduardo Ramirez
Marlene Antônia dos Reis
Lúcio Roberto Castellano
Virmondes Rodrigues
Denise Bertulucci Rocha Rodrigues
Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
BioMed Research International
author_facet Juliana Reis Machado
Marcos Vinícius Silva
Diego Costa Borges
Crislaine Aparecida da Silva
Luis Eduardo Ramirez
Marlene Antônia dos Reis
Lúcio Roberto Castellano
Virmondes Rodrigues
Denise Bertulucci Rocha Rodrigues
author_sort Juliana Reis Machado
title Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
title_short Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
title_full Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
title_fullStr Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
title_full_unstemmed Immunopathological Aspects of Experimental Trypanosoma cruzi Reinfections
title_sort immunopathological aspects of experimental trypanosoma cruzi reinfections
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2014-01-01
description Chagas disease is caused by Trypanosoma cruzi infection. Besides the host-related factors, such as immune response and genetic background, the parasite, strain, and occurrences of reinfection episodes, may influence disease outcome. Our results demonstrate that both the primary infection and the reinfection with the Colombiana strain are connected with lower survival rate of the mice. After reinfection, parasitaemia is approximately ten times lower than in primary infected animals. Only Colombiana, Colombiana/Colombiana, and Y/Colombiana groups presented amastigote nests in cardiac tissue. Moreover, the mice infected and/or reinfected with the Colombiana strain had more T. cruzi nests, more intense inflammatory infiltrate, and higher in situ expression of TNF-α and IFN-γ than Y strain. Antigen-stimulated spleen cells from infected and/or reinfected animals produced higher levels of TNF-α, IFN-γ, and IL-10. Our results reinforce the idea that Chagas disease outcome is influenced by the strain of the infective parasite, being differentially modulated during reinfection episodes. It highlights the need of control strategies involving parasite strain characterization in endemic areas for Chagas disease.
url http://dx.doi.org/10.1155/2014/648715
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