Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9943235 | The American Journal of Pathology | 2005 | 11 Pages |
Abstract
The cytokine transforming growth factor-β (TGF-β) 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-β, we observed stronger immunoreactivity in parasites than in host cells. TGF-β immunoreactivity evolved during parasite cycle progression, with intense staining in amastigotes versus very faint staining in trypomastigotes. TGF-β was present on the surface of amastigotes, in the flagellar pocket, and in intraparasitic vesicles as revealed by electron microscopy. However, no ortholog TGF-β 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-β was most probably taken up by the parasite from the host cell cytoplasm because such an internalization process of biotinylated TGF-β 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-β to control its own intracellular life cycle.
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Authors
Mariana C. Waghabi, Michelle Keramidas, Sabine Bailly, Wim Degrave, Leila Mendonça-Lima, Maria de Nazaré C. Soeiro, Maria de Nazareth L. Meirelles, Sidnei Paciornik, Tania C. Araújo-Jorge, Jean-Jacques Feige,