Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Mol Immunol ; 58(1): 92-7, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24317279

RESUMO

The recent increase in immigration of people from areas endemic for Chagas disease (Trypanosoma cruzi) to the United States and Europe has raised concerns about the transmission via blood transfusion and organ transplants in these countries. Infection by these pathways occurs through blood trypomastigotes (BT), and these forms of T. cruzi are completely distinct of metacyclic trypomastigotes (MT), released by triatomine vector, in relation to parasite-host interaction. Thus, research comparing infection with these different infective forms is important for explaining the potential impacts on the disease course. Here, we investigated tissue parasitism and relative mRNA expression of cytokines, chemokines, and chemokine receptors in the heart during acute infection by MT or BT forms in dogs. BT-infected dogs presented a higher cardiac parasitism, increased relative mRNA expression of pro-inflammatory and immunomodulatory cytokines and of the chemokines CCL3/MIP-1α, CCL5/RANTES, and the chemokine receptor CCR5 during the acute phase of infection, as compared to MT-infected dogs. These results suggest that infection with BT forms may lead to an increased immune response, as revealed by the cytokines ratio, but this kind of immune response was not able to control the cardiac parasitism. Infection with the MT form presented an increase in the relative mRNA expression of IL-12p40 as compared to that of IL-10 or TGF-ß1. Correlation analysis showed increased relative mRNA expression of IFN-γ as well as IL-10, which may be an immunomodulatory response, as well as an increase in the correlation of CCL5/RANTES and its CCR5 receptor. Our findings revealed a difference between inoculum sources of T. cruzi, as vectorial or transfusional routes of T. cruzi infection may trigger distinct parasite-host interactions during the acute phase, which may influence immunopathological aspects of Chagas disease.


Assuntos
Doença de Chagas/imunologia , Citocinas/genética , Coração/parasitologia , Miocárdio/imunologia , Trypanosoma cruzi/imunologia , Animais , Doença de Chagas/parasitologia , Quimiocina CCL3/biossíntese , Quimiocina CCL3/genética , Quimiocina CCL5/biossíntese , Quimiocina CCL5/genética , Modelos Animais de Doenças , Cães , Feminino , Interações Hospedeiro-Parasita/imunologia , Interferon gama/biossíntese , Interferon gama/genética , Interleucina-10/biossíntese , Interleucina-10/genética , Subunidade p40 da Interleucina-12/biossíntese , Subunidade p40 da Interleucina-12/genética , Masculino , Miocárdio/metabolismo , RNA Mensageiro/biossíntese , Receptores CCR5/biossíntese , Receptores CCR5/genética , Fator de Crescimento Transformador beta/biossíntese , Fator de Crescimento Transformador beta/genética
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA