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Open AccessJournal ArticleDOI

Cytosolic-free calcium elevation in Trypanosoma cruzi is required for cell invasion.

TLDR
Pretreatment of the parasites with the Ca2+ chelators quin 2 or BAPTA decreased the trypomastigotes' association to myoblasts by approximately 40 and 63%, respectively, thus indicating that an increase in intracellularCa2+ concentration in the parasites is required for cell invasion in addition to Ca2- mobilization in the host cells.
Abstract
To replicate, the trypomastigote form of Trypanosoma cruzi must invade host cells. Since a role for Ca2+ in the process of cell invasion by several intracellular parasites has been postulated, changes in the intracellular Ca2+ concentration in T. cruzi trypomastigotes and in tissue culture L6E9 myoblasts during their interaction were studied at the single cell level using digital imaging fluorescence microscopy or in cell suspensions by fluorescence spectrophotometry. An increase in cytosolic Ca2+ in T. cruzi trypomastigotes was detected at the single cell level after association of the parasites with the myoblasts. Ca2+ mobilization in the host cells was also detected upon contact with trypomastigotes either at the single cell level or in cells grown in coverslips and exposed to suspensions of trypomastigotes. Pretreatment of the parasites with the Ca2+ chelators quin 2 (50 microM) or bis-(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA, 50 microM) decreased the trypomastigotes' association to myoblasts by approximately 40 and 63%, respectively, thus indicating that an increase in intracellular Ca2+ concentration in the parasites is required for cell invasion in addition to Ca2+ mobilization in the host cells.

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Journal ArticleDOI

Trypanosoma cruzi surface mucins: host-dependent coat diversity

TL;DR: The expression profiling of T. cruzi mucins is discussed, the mechanisms leading to the acquisition of mucin diversity and the possible consequences of a mosaic surface coat in the interplay between parasite and host are discussed.
Journal ArticleDOI

Molecular basis of mammalian cell invasion by Trypanosoma cruzi

TL;DR: During MT or TCT internalization, signal transduction pathways are activated both in the parasite and the target cell, leading to Ca2+ mobilization, and T. cruzi isolate-dependent inhibitory signals, mediated by MT-specific gp90, may be triggeredboth in the host cell and the parasite.
Journal ArticleDOI

Host Cell Invasion by TRYPANOSOMA cRUZI Is Potentiated by Activation of Bradykinin B2 Receptors

TL;DR: Analysis of trypomastigote transfectants expressing various cysteine proteinase isoforms showed that invasion competence is linked to the kinin releasing activity of cruzipain, herein proposed as a factor of virulence in Chagas' disease.
Journal ArticleDOI

Oligopeptidase B-dependent signaling mediates host cell invasion by Trypanosoma cruzi

TL;DR: It is shown that deletion of the gene encoding oligopeptidase B results in a marked defect in host cell invasion and in the establishment of infections in mice, and that this enzyme is responsible for the generation of a signaling agonist for mammalian cells.
Journal ArticleDOI

Cell signalling and Trypanosoma cruzi invasion

TL;DR: Differential engagement of host cell signalling pathways in a cell type‐specific manner and modulation ofHost cell gene expression by T. cruzi are becoming recognized as essential determinants of infectivity and intracellular survival by this pathogen.
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