Open Access

ARTICLE

Trypanosoma cruzi invasion in non-phagocytic cells: an ultrastructural study

Juan Agustín CUETO³, Emile SANTOS BARRIAS⁶, Wanderley de SOUZA^{4, 5}, Patricia Silvia ROMANO^{1, 2}

1 IHEM, Universidad Nacional de Cuyo, CONICET, Laboratorio de Biología de Tripanosoma cruzi y de la célula hospedadora, Mendoza, Argentina
2 Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Área de Biología Celular y Molecular. Mendoza. Argentina
3 Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Fisiología. Mendoza. Argentina
4 Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofísica Carlos Chagas Filho, Centro de Ciência da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
5 Instituto Nacional de Ciência e Tecnologia em Biologia Estrutural e Bioimagens e Centro Nacional de Bioimagens-CENABIO, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
6 Instituto Nacional de Metrologia, Qualidade e Tecnologia-Inmetro, Rio de Janeiro, Brazil

* Address correspondence to: Juan Agustín Cueto, .

BIOCELL 2018, 42(3), 105-108. https://doi.org/10.32604/biocell.2018.07017

Abstract

Trypanosoma cruzi is the causative agent of Chagas disease. This parasite requires the intracellular niche in order to proliferate and disseminate the infection. After invasion, T. cruzi resides temporarily in an acidic vacuole which is lysed by a not well-understood mechanism. Transmission electron microscopy was used to describe the process of T. cruzi escape from the parasitophorous vacuole over the time. Using HeLa (non-professional phagocytic cells) as host cell, we observed that recently internalized parasites reside in a membrane-bounded vacuole. A few hours later, the first sign of vacuole disruption appeared as membrane discontinuities. This observation was followed by a progressive vacuole swelling as evidenced by an electron-lucent halo between the parasite and the vacuole membrane. Apparently, the vacuole membrane remnants reorganized as small vesicles that eventually disappeared from the vicinity of the parasites. Finally, parasites reach the host cell cytosol where replication takes place. The thorough ultrastructural description of this process set the base for a comprehensive understanding of the parasite-host cell interaction and, thus open the possibility of new therapeutic intervention strategies.

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