| Autor: |
Waghabi, Mariana C., Keramidas, Michelle, Bailly, Sabine, Degrave, Wim, Mendonça-Lima, Leila, Soeiro, Maria de Nazaré C., Meirelles, Maria de Nazareth L., Paciornik, Sidnei, Araújo-Jorge, Tania C., Feige, Jean-Jacques |
| Zdroj: |
American Journal of Pathology; October 2005, Vol. 167 Issue: 4 p993-1003, 11p |
| Abstrakt: |
The cytokine transforming growth factor-β (TGF-β) plays various functions in the control of Trypanosoma cruziinfectivity and in the progression of Chagas' disease. When we immunostained T. cruzi-infected cardiomyocytes (after either in vivoor in vitroinfections) 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. cruziby in silicoanalysis 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. |
| Databáze: |
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