Immunological and pathological responses in BALB/c mice induced by genetic administration of Tc13 Tul antigen of Trypanosoma cruzi

Tc13 is a trans-sialidase family protein of Trypanosoma cruzi, the aetiological agent of Chagas' disease. Recently, in vitro studies had suggested that Tc13 might participate in the pathogenesis of the disease. In order to study the role of Tc13 antigens in an in vivo model, we administered pla...

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Published inParasitology Vol. 132; no. 6; pp. 855 - 866
Main Authors GARCÍA, G. A., ARNAIZ, M. R., LAUCELLA, S. A., ESTEVA, M. I., AINCIART, N., RIARTE, A., GARAVAGLIA, P. A., FICHERA, L. E., RUIZ, A. M.
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 01.06.2006
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Summary:Tc13 is a trans-sialidase family protein of Trypanosoma cruzi, the aetiological agent of Chagas' disease. Recently, in vitro studies had suggested that Tc13 might participate in the pathogenesis of the disease. In order to study the role of Tc13 antigens in an in vivo model, we administered plasmid DNA encoding a Tc13 antigen from the Tulahuén strain (Tc13 Tul) to BALB/c mice and evaluated the immunological and pathological manifestations as well as the capacity of this antigen to confer protection against T. cruzi infection. Tc13 Tul immunization did not elicit a detectable humoral immune response but induced specific memory T-cells with no capacity to produce IFN-γ. Five months after DNA-immunization with Tc13 Tul, signs of hepatotoxicity and reactive changes in the heart, liver and spleen were observed in 40–80% of mice. When Tc13 Tul DNA-immunized animals were challenged with trypomastigotes, a significant decrease in parasitaemia in early and late acute phase was observed without modification in the survival rate. Surprisingly, Tc13 Tul-immunized mice chronically infected with T. cruzi showed a decrease in the severity of heart damage. We conclude that, in BALB/c mice, genetic immunization with Tc13 Tul mainly induces immune responses associated with pathology.
Bibliography:istex:1907C4060C29A9CD94BDDCC31FB54AA293BF8D15
PMID:16478565
PII:S0031182005009753
ark:/67375/6GQ-C66P9BMT-C
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0031-1820
1469-8161
DOI:10.1017/S0031182005009753