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Molecular and cellular mechanisms involved in the Trypanosoma cruzi /host cell interplay
Author(s) -
Romano Patricia Silvia,
Cueto Juan Agustín,
Casassa Ana Florencia,
Vanrell María Cristina,
Gottlieb Roberta A.,
Colombo María Isabel
Publication year - 2012
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1019
Subject(s) - trypanosoma cruzi , microbiology and biotechnology , biology , vacuole , autophagy , phagocytosis , context (archaeology) , downregulation and upregulation , infectivity , cell , parasite hosting , immunology , biochemistry , cytoplasm , gene , virus , apoptosis , paleontology , world wide web , computer science
The protozoan parasite Trypanosoma cruzi has a complex biological cycle that involves vertebrate and invertebrate hosts. In mammals, the infective trypomastigote form of this parasite can invade several cell types by exploiting phagocytic‐like or nonphagocytic mechanisms depending on the class of cell involved. Morphological studies showed that when trypomastigotes contact macrophages, they induce the formation of plasma membrane protrusions that differ from the canonical phagocytosis that occurs in the case of noninfective epimastigotes. In contrast, when trypomastigotes infect epithelial or muscle cells, the cell surface is minimally modified, suggesting the induction of a different class of process. Lysosomal‐dependent or ‐independent T. cruzi invasion of host cells are two different models that describe the molecular and cellular events activated during parasite entry into nonphagocytic cells. In this context, we have previously shown that induction of autophagy in host cells before infection favors T. cruzi invasion. Furthermore, we demonstrate that autophagosomes and the autophagosomal protein LC3 are recruited to the T. cruzi entry sites and that the newly formed T. cruzi parasitophorous vacuole has characteristics of an autophagolysosome. This review summarizes the current knowledge of the molecular and cellular mechanisms of T. cruzi invasion in nonphagocytic cells. Based on our findings, we propose a new model in which T. cruzi takes advantage of the upregulation of autophagy during starvation to increase its successful colonization of host cells. 2012 IUBMB IUBMB Life, 2012