Trypanosoma cruzi-cardiomyocytes: new contributions regarding a better understanding of this interaction

Meirelles, Maria de Nazareth Leal de; Pereira, Mirian Cláudia de Souza; Singer, Robert H.; Soeiro, Maria de Nazaré Correia; Garzoni, Luciana Ribeiro; Silva, Dayse T.; Barbosa, Helene Santos; Araújo-Jorge, Tânia C.; Masuda, Masako Oya; Capella, Marcia A. M.; Lopes, Anibal Gil; Vermelho, Alane Beatriz

doi:10.1590/s0074-02761999000700017

Cited by 20 publications

(15 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…6A and B). This apparent lack of good quality control is explained by the known effects of intense T. cruzi infection on heart muscle cells, where the disruption of the actin cytoskeleton generates an increase in ␤-actin production (39). This observation is consistent with the higher parasite burdens and severe pathology in the infected hearts of MIF Ϫ/Ϫ mice.…”

Section: T Cruzi-infected Mifmentioning

confidence: 55%

Macrophage Migration Inhibitory Factor Contributes to Host Defense against AcuteTrypanosoma cruziInfection

Reyes

Terrazas

Espinoza³

et al. 2006

Infect Immun

View full text Add to dashboard Cite

show abstract

Section: T Cruzi-infected Mifmentioning

confidence: 55%

Macrophage Migration Inhibitory Factor Contributes to Host Defense against AcuteTrypanosoma cruziInfection

Reyes

Terrazas

Espinoza³

et al. 2006

Infect Immun

View full text Add to dashboard Cite

show abstract

“…Trypomastigotes loaded with BCECF-AM could be easily visualized attached to cardiomyocyte surface. Calcium responses are critically required for invasion of cardiomyocytes as shown with other cell types (Osuna et al 1990, Moreno et al 1994, Tardieux et al 1994, Dorta et al 1995, Meirelles et al 1999, Scharfstein et al 2000. Thapsigargin sensible sarcoplasmic reticulum Ca 2+ -ATPase (SERCA) was involved in T. cruzi invasion on coupled cardiomyocytes since the treatment of HMC with this drug inhibited parasite invasion (Meirelles et al 1999, Todorov et al 2003.…”

Section: Discussionmentioning

confidence: 98%

Characterization of [Ca2+]i responses in primary cultures of mouse cardiomyocytes induced by Trypanosoma cruzi trypomastigotes

Garzoni

Masuda

Capella³

et al. 2003

Mem. Inst. Oswaldo Cruz

Self Cite

View full text Add to dashboard Cite

“…Although T. cruzi has the capacity to infect the majority of the cells, it was demonstrated that cardiac and smooth muscle myocytes are the more susceptible cells to this parasitic infection (52,53). Indeed, heart or digestive lesions characterize the chronic stage of Chagas disease (54).…”

Section: The Autophagic Model Of T Cruzi Invasionmentioning

confidence: 99%

Molecular and cellular mechanisms involved in the trypanosoma cruzi/host cell interplay

et al. 2012

View full text Add to dashboard Cite

SummaryThe protozoan parasite Trypanosoma cruzi has a complex bi-ological 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 non-phagocytic 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 up-regulation of autophagy during starvation to increase its successful colonization of host cells.

show abstract

Trypanosoma cruzi-cardiomyocytes: new contributions regarding a better understanding of this interaction

Cited by 20 publications

References 20 publications

Macrophage Migration Inhibitory Factor Contributes to Host Defense against AcuteTrypanosoma cruziInfection

Macrophage Migration Inhibitory Factor Contributes to Host Defense against AcuteTrypanosoma cruziInfection

Characterization of [Ca2+]i responses in primary cultures of mouse cardiomyocytes induced by Trypanosoma cruzi trypomastigotes

Molecular and cellular mechanisms involved in the trypanosoma cruzi/host cell interplay

Contact Info

Product

Resources

About