Trypanosoma cruzi trypomastigotes induce cytoskeleton modifications during HeLa cell invasion

Fernandes, Maria Cecília; Andrade, Leonardo R.; Andrews, Norma W.; Mortara, Renato Arruda

doi:10.1590/s0074-02762011000800019

Cited by 12 publications

(11 citation statements)

References 10 publications

(9 reference statements)

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“…During cell infection, T . cruzi uses the cell membrane repair mechanism to promote its internalization in non-professional phagocytic cells, forming a vacuole containing lysosomal markers and content [ 46 , 47 ]. The acidic content of the vacuole allows the parasite to gradually escape into the cytoplasm of the cell, where it completes its transformation into the amastigote form and initiates its intracellular multiplication [ 15 , 48 – 51 ].…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocyte oxidants production may signal to T. cruzi intracellular development

et al. 2017

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Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, presents a variable clinical course, varying from asymptomatic to serious debilitating pathologies with cardiac, digestive or cardio-digestive impairment. Previous studies using two clonal T. cruzi populations, Col1.7G2 (T. cruzi I) and JG (T. cruzi II) demonstrated that there was a differential tissue distribution of these parasites during infection in BALB/c mice, with predominance of JG in the heart. To date little is known about the mechanisms that determine this tissue selection. Upon infection, host cells respond producing several factors, such as reactive oxygen species (ROS), cytokines, among others. Herein and in agreement with previous data from the literature we show that JG presents a higher intracellular multiplication rate when compared to Col1.7G2. We also showed that upon infection cardiomyocytes in culture may increase the production of oxidative species and its levels are higher in cultures infected with JG, which expresses lower levels of antioxidant enzymes. Interestingly, inhibition of oxidative stress severely interferes with the intracellular multiplication rate of JG. Additionally, upon H2O2-treatment increase in intracellular Ca2+ and oxidants were observed only in JG epimastigotes. Data presented herein suggests that JG and Col1.7G2 may sense extracellular oxidants in a distinct manner, which would then interfere differently with their intracellular development in cardiomyocytes.

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Section: Discussionmentioning

confidence: 99%

Cardiomyocyte oxidants production may signal to T. cruzi intracellular development

et al. 2017

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“…These results showed that T. cruzi EAs trigger a markedly different invasion pathway than the flagellated tissue culture trypomastigotes (Procópio et al, 1998), which do not rely on host cell actin polymerization to enter host cells (Schenkman et al, 1991;Tardieux et al, 1992;Fernandes et al, 2011a). Trypomastigotes were shown to wound the host cell and to take advantage of the plasma membrane repair mechanism which involves lysosomal exocytosis and subsequent endocytosis (Fernandes et al, 2011b).…”

Section: T Cruzi Eas Trigger Formation Of Structures Rich In Polymermentioning

confidence: 98%

Extracellular amastigotes ofTrypanosoma cruziare potent inducers of phagocytosis in mammalian cells

et al. 2013

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The protozoan parasite Trypanosoma cruzi, the aetiological agent of Chagas' disease, has two infective life cycle stages, trypomastigotes and amastigotes. While trypomastigotes actively enter mammalian cells, highly infective extracellular amastigotes (type I T. cruzi) rely on actin-mediated uptake, which is generally inefficient in non-professional phagocytes. We found that extracellular amastigotes (EAs) of T. cruzi G strain (type I), but not Y strain (type II), were taken up 100-fold more efficiently than inert particles. Mammalian cell lines showed levels of parasite uptake comparable to macrophages, and extensive actin recruitment and polymerization was observed at the site of entry. EA uptake was not dependent on parasite-secreted molecules and required the same molecular machinery utilized by professional phagocytes during large particle phagocytosis. Transcriptional silencing of synaptotagmin VII and CD63 significantly inhibited EA internalization, demonstrating that delivery of supplemental lysosomal membrane to form the phagosome is involved in parasite uptake. Importantly, time-lapse live imaging using fluorescent reporters revealed phagosome-associated modulation of phosphoinositide metabolism during EA uptake that closely resembles what occurs during phagocytosis by macrophages. Collectively, our results demonstrate that T. cruzi EAs are potent inducers of phagocytosis in non-professional phagocytes, a process that may facilitate parasite persistence in infected hosts.

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“…(iii) Activated signaling pathways also participate, including tyrosine kinase receptors (TrKA and TrKC; de Melo-Jorge and PereiraPerrin, 2007; Weinkauf et al, 2011) and phosphatidylinositol 3-kinase (PI3-K; Todorov et al, 2000; Chuenkova et al, 2001; Wilkowsky et al, 2001; Vieira et al, 2002; Woolsey et al, 2003), bradykinin receptors (Scharfstein et al, 2000; Todorov et al, 2003), and transforming growth factor β (TGF-β; Ming et al, 1995; Waghabi et al, 2007). (iv) More recently, sphingomyelinase-mediated plasma membrane repair has been proposed to participate in this process (Fernandes et al, 2011; Fernandes and Andrews, 2012), as has (v) the host cell autophagy pathway (Romano et al, 2009, 2012). Finally, the combination of different mechanisms has been described as coordinating the T. cruzi invasion process (Butler and Tyler, 2012).…”

Section: Cell Recognition and Invasion Processmentioning

confidence: 99%

Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction

Calvet¹,

Melo²,

Garzoni³

et al. 2012

Front. Immun.

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Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits multiple strategies to ensure its establishment and persistence in the host. Although this parasite has the ability to infect different organs, heart impairment is the most frequent clinical manifestation of the disease. Advances in knowledge of T. cruzi–cardiomyocyte interactions have contributed to a better understanding of the biological events involved in the pathogenesis of Chagas disease. This brief review focuses on the current understanding of molecules involved in T. cruzi–cardiomyocyte recognition, the mechanism of invasion, and on the effect of intracellular development of T. cruzi on the structural organization and molecular response of the target cell.

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Trypanosoma cruzi trypomastigotes induce cytoskeleton modifications during HeLa cell invasion

Cited by 12 publications

References 10 publications

Cardiomyocyte oxidants production may signal to T. cruzi intracellular development

Cardiomyocyte oxidants production may signal to T. cruzi intracellular development

Extracellular amastigotes ofTrypanosoma cruziare potent inducers of phagocytosis in mammalian cells

Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction

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