Recently differentiated epimastigotes from Trypanosoma cruzi are infective to the mammalian host.

Abstract:

:Trypanosoma cruzi, the etiologic agent of Chagas disease, has a complex life cycle in which four distinct developmental forms alternate between the insect vector and the mammalian host. It is assumed that replicating epimastigotes present in the insect gut are not infective to mammalian host, a paradigm corroborated by the widely acknowledged fact that only this stage is susceptible to the complement system. In the present work, we establish a T. cruzi in vitro and in vivo epimastigogenesis model to analyze the biological aspects of recently differentiated epimastigotes (rdEpi). We show that both trypomastigote stages of T. cruzi (cell-derived and metacyclic) are able to transform into epimastigotes (processes termed primary and secondary epimastigogenesis, respectively) and that rdEpi have striking properties in comparison to long-term cultured epimastigotes: resistance to complement-mediated lysis and both in vitro (cell culture) and in vivo (mouse) infectivity. Proteomics analysis of all T. cruzi stages reveled a cluster of proteins that were up-regulated only in rdEpi (including ABC transporters and ERO1), suggesting a role for them in rdEpi virulence. The present work introduces a new experimental model for the study of host-parasite interactions, showing that rdEpi can be infective to the mammalian host.

journal_name

Mol Microbiol

journal_title

Molecular microbiology

authors

Kessler RL,Contreras VT,Marliére NP,Aparecida Guarneri A,Villamizar Silva LH,Mazzarotto GACA,Batista M,Soccol VT,Krieger MA,Probst CM

doi

10.1111/mmi.13653

subject

Has Abstract

pub_date

2017-06-01 00:00:00

pages

712-736

issue

5

eissn

0950-382X

issn

1365-2958

journal_volume

104

pub_type

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