Extracellular vesicles isolated from Trypanosoma cruzi affect early parasite migration in the gut of Rhodnius prolixus but not in Triatoma infestans

Paranaíba, Larissa Ferreira; Guarneri, Alessandra A.; Torrecilhas, Ana Claúdia; Melo, Maria Norma; Soares, Rodrigo Pedro

doi:10.1590/0074-02760190217

Cited by 14 publications

(13 citation statements)

References 19 publications

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“…EVs are produced by the different life stages of T. cruzi ( da Silveira et al, 1979 ; Gonçalves et al, 1991 ; Cestari et al, 2012 ; Bayer-Santos et al, 2013 ; Nogueira et al, 2015 ; Ramirez et al, 2017 ; Caeiro et al, 2018 ; Ribeiro et al, 2018 ; Paranaiba et al, 2019 ; Rossi et al, 2019 ) and participate in parasite host interactions ( Marcilla et al, 2014 ; De Pablos et al, 2016 ; Diaz Lozano et al, 2017 ; Ramirez et al, 2017 ; Wyllie and Ramirez, 2017 ; de Pablos Torro et al, 2018 ; Retana Moreira et al, 2019 ; Cronemberger-Andrade et al, 2020 ). Figure 1 illustrates EVs in different T. cruzi life stages.…”

Section: T Cruzi Evsmentioning

confidence: 99%

“…The lack of studies of amastigote EVs is expected since it’s intracellular location and the secreted material as it is often contaminated with host cell constituents. In both epimastigotes and trypomastigotes, EVs contain several surface components of the parasite involved in the parasite adhesion, invasion, and migration in the vector’s gut ( Nogueira et al, 2015 ; Ribeiro et al, 2018 ; Paranaiba et al, 2019 ; Cronemberger-Andrade et al, 2020 ). Trypomastigote EVs modulates T. cruzi infection and affect the protozoan ability to enter and escape the parasitophorous vacuole.…”

Section: T Cruzi Evsmentioning

confidence: 99%

“…EVs were artificially offered to the insects prior to infection with epimastigotes. Pre-feeding with EVs delayed early parasite migration to the rectum in R. prolixus , but not in T. infestans , affecting parasite-host interaction during the initial events of infection in the invertebrate’s gut ( Paranaiba et al, 2019 ). However, the mechanisms underlying parasite retainment remain to be explored.…”

Section: T Cruzi Evsmentioning

confidence: 99%

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Extracellular Vesicles in Trypanosomatids: Host Cell Communication

Torrecilhas

Soares

Schenkman

et al. 2020

Front. Cell. Infect. Microbiol.

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Trypanosoma cruzi, Trypanosoma brucei and Leishmania (Trypanosomatidae: Kinetoplastida) are parasitic protozoan causing Chagas disease, African Trypanosomiasis and Leishmaniases worldwide. They are vector borne diseases transmitted by triatomine bugs, Tsetse fly, and sand flies, respectively. Those diseases cause enormous economic losses and morbidity affecting not only rural and poverty areas but are also spreading to urban areas. During the parasite-host interaction, those organisms release extracellular vesicles (EVs) that are crucial for the immunomodulatory events triggered by the parasites. EVs are involved in cell-cell communication and can act as important pro-inflammatory mediators. Therefore, interface between EVs and host immune responses are crucial for the immunopathological events that those diseases exhibit. Additionally, EVs from these organisms have a role in the invertebrate hosts digestive tracts prior to parasite transmission. This review summarizes the available data on how EVs from those medically important trypanosomatids affect their interaction with vertebrate and invertebrate hosts.

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Section: T Cruzi Evsmentioning

confidence: 99%

Section: T Cruzi Evsmentioning

confidence: 99%

Section: T Cruzi Evsmentioning

confidence: 99%

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Extracellular Vesicles in Trypanosomatids: Host Cell Communication

Torrecilhas

Soares

Schenkman

et al. 2020

Front. Cell. Infect. Microbiol.

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“…A study with EVs derived from epimastigotes indicated that they promoted the differentiation of the replicative forms into MTs ( Garcia-Silva et al., 2014 ). In another study, purified EVs from epimastigotes, given to two distinct triatomine insects prior to infection with epimastigotes, affected early parasite migration in the gut of Rhodnius prolixus but not in Triatoma infestans ( Paranaiba et al., 2019 ). As regards TCT, EVs derived from different T. cruzi strains were shown to trigger differential innate and chronic immune responses ( Nogueira et al., 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Shedding of Trypanosoma cruzi Surface Molecules That Regulate Host Cell Invasion Involves Phospholipase C and Increases Upon Sterol Depletion

Loch

Onofre

Rodrigues

et al. 2021

Front. Cell. Infect. Microbiol.

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Metacyclic trypomastigote (MT) forms of Trypanosoma cruzi have been shown to release into medium gp82 and gp90, the stage-specific surface molecules that regulate host cell invasion, either in vesicles or in soluble form. Here, we found that during interaction of poorly invasive G strain with the host cell, gp82 and gp90 were released in vesicle-like forms, whereas no such release by highly invasive CL strain was observed. Shedding of vesicles of varying sizes by CL and G strains was visualized by scanning electron microscopy, and the protein profile of conditioned medium (CM) of the two strains was similar, but the content of gp82 and gp90 differed, with both molecules being detected in G strain as bands of high intensity in Western blotting, whereas in CL strain, they were barely detectable. Confocal images revealed a distinct distribution of gp82 and gp90 on MT surface of CL and G strains. In cell invasion assays, addition of G strain CM resulted in decreased CL strain internalization. Depletion of gp82 in G strain CM, by treatment with specific mAb-coupled magnetic beads, increased its inhibitory effect on CL strain invasion, in contrast to CM depleted in gp90. The effect of cholesterol-depleting drug methyl-β-cyclodextrin (MβCD) on gp82 and gp90 release by MTs was also examined. G strain MTs, untreated or treated with MβCD, were incubated in serum-containing medium or in nutrient-depleted PBS++, and the CM generated under these conditions was analyzed by Western blotting. In PBS++, gp82 and gp90 were released at lower levels by untreated MTs, as compared with MβCD-treated parasites. CM from untreated and MβCD-treated G strain, generated in PBS++, inhibited CL strain internalization. Treatment of CL strain MTs with MβCD resulted in increased gp82 and gp90 shedding and in decreased host cell invasion. The involvement of phospholipase C (PLC) on gp82 and gp90 shedding was also investigated. The CM from G strain MTs pretreated with specific PLC inhibitor contained lower levels of gp82 and gp90, as compared with untreated parasites. Our results contribute to shed light on the mechanism by which T. cruzi releases surface molecules implicated in host cell invasion.

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“…Previous studies have already shown that different stages of T. cruzi release EVs under physiological conditions. They modulate NO and cytokine production by macrophages and delay parasite migration in the gut of vector [29,30]. Here, several experiments evaluated the role of stress factors affecting EV release by T. cruzi trypomastigotes.…”

Section: Discussionmentioning

confidence: 99%

Stress Induces Release of Extracellular Vesicles by Trypanosoma cruzi Trypomastigotes

Vasconcelos

Andrade

Souza-Melo

et al. 2021

Journal of Immunology Research

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All extracellular forms of Trypanosoma cruzi, the causative agent of Chagas disease, release extracellular vesicles (EVs) containing major surface molecules of the parasite. EV release depends on several mechanisms (internal and external). However, most of the environmental conditions affecting this phenomenon are still unknown. In this work, we evaluated EV release under different stress conditions and their ability to be internalized by the parasites. In addition, we investigated whether the release conditions would affect their immunomodulatory properties in preactivated bone marrow-derived macrophages (BMDM). Sodium azide and methyl-cyclo-β-dextrin (CDB) reduced EV release, indicating that this phenomenon relies on membrane organization. EV release was increased at low temperatures (4°C) and acidic conditions (pH 5.0). Under this pH, trypomastigotes differentiated into amastigotes. EVs are rapidly liberated and reabsorbed by the trypomastigotes in a concentration-dependent manner. Nitrosative stress caused by sodium nitrite in acid medium or S-nitrosoglutathione also stimulated the secretion of EVs. EVs released under all stress conditions also maintained their proinflammatory activity and increased the expression of iNOS, Arg 1, IL-12, and IL-23 genes in IFN-γ and LPS preactivated BMDM. In conclusion, our results suggest a budding mechanism of release, dependent on the membrane structure and parasite integrity. Stress conditions did not affect functional properties of EVs during interaction with host cells. EV release variations under stress conditions may be a physiological response against environmental changes.

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Extracellular vesicles isolated from Trypanosoma cruzi affect early parasite migration in the gut of Rhodnius prolixus but not in Triatoma infestans

Cited by 14 publications

References 19 publications

Extracellular Vesicles in Trypanosomatids: Host Cell Communication

Extracellular Vesicles in Trypanosomatids: Host Cell Communication

Shedding of Trypanosoma cruzi Surface Molecules That Regulate Host Cell Invasion Involves Phospholipase C and Increases Upon Sterol Depletion

Stress Induces Release of Extracellular Vesicles by Trypanosoma cruzi Trypomastigotes

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