Trypanosoma cruzi cell invasion and traffic: Influence of Coxiella burnetii and pH in a comparative study between distinct infective forms

Fernandes, Maria Cecília; L’Abbate, Carolina; Andreoli, Walter K.; Mortara, Renato Arruda

doi:10.1016/j.micpath.2007.02.005

Cited by 8 publications

(8 citation statements)

References 59 publications

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“…It was previously shown that EAs from different T. cruzi strains vary in their capacity to enter mammalian cells (Fernandes and Mortara, 2004;Fernandes et al, 2007a). In order to determine if secreted molecules from the G strain were involved, we exposed HeLa cells to a mixed population of GFP-tagged Y strain (type II) and untagged G strain (type I) EAs and quantified the number of internalized parasites in HeLa cells under different conditions (Fig.…”

Section: Phagocytic Uptake Induced By T Cruzi Eas Requires Intact Sumentioning

confidence: 99%

“…EAs from group I T. cruzi strains (such as the G strain) were found to enter mammalian cells much more efficiently than group II (Y strain) or VI (CL strain) parasites (Fernandes and Mortara, ; Mortara et al ., ; da Silva et al ., ; Fernandes et al ., ; Bambino‐Medeiros et al ., ; Rodrigues et al ., ). Further studies revealed that EAs of either G or Y strains are capable of initiating infections in a wide range of mammalian cells and, as the flagellated trypomastigotes, elicit responses from the host cell (Fernandes and Mortara, ; Fernandes et al ., ; Fernandes et al ., ,b; Cruz et al . , ).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Phagocytic Uptake Induced By T Cruzi Eas Requires Intact Sumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Extracellular amastigotes ofTrypanosoma cruziare potent inducers of phagocytosis in mammalian cells

et al. 2013

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“…4; also see Movie S4). Rab7 is a marker of late endosomes and phagolysosomes, which can be observed in the membrane of PVs formed by L. amazonensis or T. cruzi in the first few hours postinfection in vitro (47,73). At the beginning of our recordings, MT forms could be seen surrounded by Rab7; a flagellum also could be inferred from Rab7 contours (Fig.…”

Section: Resultsmentioning

confidence: 73%

“…Based on the fusogenic characteristic of T. cruzi metacyclic vacuoles, an additional study investigated the fate of metacyclic trypomastigotes within C. burnetii vacuoles, revealing that after 12 h postinfection, metacyclic trypomastigotes began to differentiate into amastigotes that replicated and became the prevailing form within C. burnetii vacuoles (35). In addition, a study comparing the ability of two T. cruzi strains to invade cells harboring C. burnetii and escape from their vacuoles suggested that despite a contrasting difference in their invasion capabilities, these strains behaved similarly once inside the host cell (47).…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma cruzi Differentiates and Multiplies within Chimeric Parasitophorous Vacuoles in Macrophages Coinfected with Leishmania amazonensis

et al. 2016

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The trypanosomatids Leishmania amazonensis and Trypanosoma cruzi are excellent models for the study of the cell biology of intracellular protozoan infections. After their uptake by mammalian cells, the parasitic protozoan flagellates L. amazonensis and T. cruzi lodge within acidified parasitophorous vacuoles (PVs). However, whereas L. amazonensis develops in spacious, phagolysosome-like PVs that may enclose numerous parasites, T. cruzi is transiently hosted within smaller vacuoles from which it soon escapes to the host cell cytosol. To investigate if parasite-specific vacuoles are required for the survival and differentiation of T. cruzi, we constructed chimeric vacuoles by infection of L. amazonensis amastigote-infected macrophages with T. cruzi epimastigotes (EPIs) or metacyclic trypomastigotes (MTs). These chimeric vacuoles, easily observed by microscopy, allowed the entry and fate of T. cruzi in L. amazonensis PVs to be dynamically recorded by multidimensional imaging of coinfected cells. We found that although T. cruzi EPIs remained motile and conserved their morphology in chimeric vacuoles, T. cruzi MTs differentiated into amastigote-like forms capable of multiplying. These results demonstrate that the large adaptive vacuoles of L. amazonensis are permissive to T. cruzi survival and differentiation and that noninfective EPIs are spared from destruction within the chimeric PVs. We conclude that T. cruzi differentiation can take place in Leishmania-containing vacuoles, suggesting this occurs prior to their escape into the host cell cytosol.

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“…It is known that several intracellular pathogens such as Listeria, Shigella , Ricketsia, and Trypanossoma cruzi [83, 84] translocate to the cytosol in order to avoid degradation within the phagolysosome. This phenomenon was also described for M. marinum , which causes tuberculosis-like disease in their natural hosts, fish and frog [120] and “fish tank granuloma”, a granulomatous skin syndrome, among humans [121].…”

Section: Mycobacteria Persistence and Host Defence Mechanismsmentioning

confidence: 99%

Tuberculosis: New Aspects of an Old Disease

Jordão

Vieira

2011

International Journal of Cell Biology

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Tuberculosis is an ancient infectious disease that remains a threat for public health around the world. Although the etiological agent as well as tuberculosis pathogenesis is well known, the molecular mechanisms underlying the host defense to the bacilli remain elusive. In this paper we focus on the innate immunity of this disease reviewing well-established and consensual mechanisms like Mycobacterium tuberculosis interference with phagosome maturation, less consensual mechanism like nitric oxide production, and new mechanisms, such as mycobacteria translocation to the cytosol, autophagy, and apoptosis/necrosis proposed mainly during the last decade.

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Trypanosoma cruzi cell invasion and traffic: Influence of Coxiella burnetii and pH in a comparative study between distinct infective forms

Cited by 8 publications

References 59 publications

Extracellular amastigotes ofTrypanosoma cruziare potent inducers of phagocytosis in mammalian cells

Extracellular amastigotes ofTrypanosoma cruziare potent inducers of phagocytosis in mammalian cells

Trypanosoma cruzi Differentiates and Multiplies within Chimeric Parasitophorous Vacuoles in Macrophages Coinfected with Leishmania amazonensis

Tuberculosis: New Aspects of an Old Disease

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