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Uptake of host cell transforming growth factor-beta by Trypanosoma cruzi amastigotes in cardiomyocytes: potential role in parasite cycle completion.


ABSTRACT: The cytokine transforming growth factor-beta (TGF-beta) plays various functions in the control of Trypanosoma cruzi infectivity and in the progression of Chagas' disease. When we immunostained T. cruzi-infected cardiomyocytes (after either in vivo or in vitro infections) for TGF-beta, we observed stronger immunoreactivity in parasites than in host cells. TGF-beta immunoreactivity evolved during parasite cycle progression, with intense staining in amastigotes versus very faint staining in trypomastigotes. TGF-beta was present on the surface of amastigotes, in the flagellar pocket, and in intraparasitic vesicles as revealed by electron microscopy. However, no ortholog TGF-beta gene could be identified in the genome of T. cruzi by in silico analysis or by extensive polymerase chain reaction and reverse transcriptase-polymerase chain reaction studies. Immunoreactive TGF-beta was most probably taken up by the parasite from the host cell cytoplasm because such an internalization process of biotinylated TGF-beta could be observed in axenic amastigotes in vitro. These observations represent the first example of a novel mechanism by which a primitive unicellular protozoan can use host cell TGF-beta to control its own intracellular life cycle.

SUBMITTER: Waghabi MC 

PROVIDER: S-EPMC1603686 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature

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Uptake of host cell transforming growth factor-beta by Trypanosoma cruzi amastigotes in cardiomyocytes: potential role in parasite cycle completion.

Waghabi Mariana C MC   Keramidas Michelle M   Bailly Sabine S   Degrave Wim W   Mendonça-Lima Leila L   Soeiro Maria de Nazaré C Mde N   Meirelles Maria de Nazareth L Mde N   Paciornik Sidnei S   Araújo-Jorge Tania C TC   Feige Jean-Jacques JJ  

The American journal of pathology 20051001 4


The cytokine transforming growth factor-beta (TGF-beta) plays various functions in the control of Trypanosoma cruzi infectivity and in the progression of Chagas' disease. When we immunostained T. cruzi-infected cardiomyocytes (after either in vivo or in vitro infections) for TGF-beta, we observed stronger immunoreactivity in parasites than in host cells. TGF-beta immunoreactivity evolved during parasite cycle progression, with intense staining in amastigotes versus very faint staining in trypoma  ...[more]

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