Decreased cruzipain and gp85/trans-sialidase family protein expression contributes to loss of Trypanosoma cruzi trypomastigote virulence

Francisco, Juan San; Barría, Iván; Gutiérrez, Bessy; Neira, Iván; Muñoz, Christian; Sagua, H; Araya, Jorge E.; Andrade, Juan Carlos Martínez; Zailberger, Anibal; Catalán, Alejandro; Remonsellez, Francisco; Vega, José Luis; González, Jorge

doi:10.1016/j.micinf.2016.08.003

Cited by 31 publications

(35 citation statements)

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“…21,22 This strain is classified in the group TcIa of DTU. 18 A clone of this strain was maintained in alternate mouse-cell culture passage whereas another clone was maintained in axenic culture passage, which generated two clones of the same strain, one highly virulent (C8C3hvir) and one with very low virulence (C8C3lvir). 18 This allowed us to infer that the effect on the Panx1 channel must be mediated by a virulence factor because avirulent cell line (C8C3lvir) did not modify Panx1 channel activity.…”

Section: Discussionmentioning

confidence: 99%

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Trypanosoma cruzi Infection Induces Pannexin-1 Channel Opening in Cardiac Myocytes

Barría

Güiza

Cifuentes

et al. 2018

The American Journal of Tropical Medicine and Hygiene

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, the etiological agent of Chagas diseases, invades the cardiac tissue causing acute myocarditis and heart electrical disturbances. In invasion, the parasite induces [Ca] transients in the host cells, an essential phenomenon for invasion. To date, knowledge on the mechanism that elicits transients of [Ca] during the infection of cardiac myocytes has not been fully characterized. Pannexin1 (Panx1) channel are poorly selective channels found in all vertebrates that serve as a pathway for ATP release. In this article, we demonstrate that infection results in the opening of Panx1 channels in cardiac myocytes. We show that pharmacological blockade of Panx1 channels inhibits-induced [Ca] transients and invasion in cardiac myocytes. Our results indicate that opening of Panx1 channels are required for invasion in cardiac myocytes, and we propose that targeting Panx1 channel could provide new potential therapeutic approaches to treat Chagas disease.

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Section: Discussionmentioning

confidence: 99%

“…17 Trypanosoma cruzi-virulent clone (H510 C8C3hvir) were maintained for 30 years in an alternate mouse-cell culture passage, and avirulent clones (H510 C8C3lvir) were maintained for 30 years in an axenic culture passage. 18 Epimastigote forms were grown at 27°C in LIT medium (containing 5.4 mM KCl, 150 mM NaCl, 24 mM glucose, 5%…”

Section: Methodsmentioning

confidence: 99%

Trypanosoma cruzi Infection Induces Pannexin-1 Channel Opening in Cardiac Myocytes

Barría

Güiza

Cifuentes

et al. 2018

The American Journal of Tropical Medicine and Hygiene

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“…Todeschini and colleagues [39] demonstrated that inactive enzymes of the TS family are sialic acid-binding proteins and terminal β-galactopyranose (βGalp) residues. In relation to gp85/transsialidase, San Francisco and colleagues [40] demonstrate that this protein plays a fundamental importance in invasion since its depletion causes a decrease in T. cruzi virulence. The same type of result was reported by Pascuale et al [41] since inactive TS expression in trypomastigotes of a strain that does not express these TS (iTS null) allowed a better invasion and increase of the parasitic load in mice demonstrating that the inactive form may act alternatively or complementing the active TS in pathogenesis.…”

Section: T Cruzi Trypomastigote-host Cell Recognitionmentioning

confidence: 99%

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

Barrias¹,

Reignault²,

Souza³

2019

Biology OfTrypanosoma Cruzi

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Trypanosoma cruzi, the etiological agent of Chagas disease, is an intracellular parasite that targets specific proteins of the host cell resulting in the generation of a unique parasitophorous vacuole (PV). As an intracellular parasite, T. cruzi interacts with cells from the mammalian host. Here we review aspects related with the binding of the main infective developmental stage (trypomastigote) to the host cell and its recognition by surface-exposed ligands/receptors. This process involves numerous signaling pathways and culminates in the entry of the parasite and modifications in both cells. The invasion of trypomastigotes occurs through multiple endocytic process, assembly of the PV, interaction of this vacuole with the endolysosomal system, lysis of the PV membrane, and multiplication of amastigotes within the cell in direct contact with host cell organelles.assumed that replicating epimastigotes present in the insect gut are not infective to mammalian host. During the vector infection (caused by a hematophagous insect of the family Reduviidae), metacyclic trypomastigotes [8], which penetrate the vertebrate host (several mammals, including man), are released along with their excreta coming in contact with conjunctiva areas or through small lesions in the own site of the bite (favored by the itch caused after the insect's bite). In turn, metacyclic trypomastigotes are able to invade virtually all cell types in the vertebrate host, especially muscle cells, fibroblasts, and macrophages [6]. At this moment, the intracellular cycle of T. cruzi begins, where the firing of several signaling cascades culminates with the closure of the parasitophorous vacuole (PV) where the parasite is found [9,10]. After the PV closure, the process of differentiation of the parasite from the trypomastigote stage to the amastigote stage begins. At the same time, fragmentation of the PV membrane takes place most probably due to the increased concentration of the Tc-Tox perforin-like protein produced by the parasite [11]. After the destruction of the vacuole, the parasite, in the process of differentiation, will be found in the cytoplasm of the host cell where it will initiate its multiplication and subsequent differentiation for trypomastigotes culminating in the rupture of the host cell (Figure 1) [13]. The whole process of formation of the parasitophorous vacuole until its rupture counts on the participation of several organelles of the host cell. Among these, the best characterized is the participation of host cell endosomes and lysosomes. It is the fusion of these organelles with the PV membrane that probably allows the increase or expansion of the PV. In addition, this process is also responsible for the generation of an acidic environment within the PV, which probably will potentiate the action of Tc-Tox and PV membrane fragmentation [13]. Wilkowsky and colleagues [14] have shown that early and late endosomes were critical for vacuole formation. In addition, other organelles responsible for the production of proteins and energy (...

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“…Due to its importance, this variable should be taken into account for experimental design. Besides, the parasite strains show different virulence relying on virulence factors such as trans-sialidase activity, complement resistance, and cysteine protease cruzipain (TCC) [18]. Trans-sialidase removes and transfers sialic acid from host cells to parasite mucinlike glycoprotein.…”

Section: Chagas Disease -Basic Investigations and Challenges 12mentioning

confidence: 99%

Biochemical, Cellular, and Immunologic Aspects during Early Interaction between Trypanosoma cruzi and Host Cell

Solís-Oviedo¹,

Monteón²,

López³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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The close parasite-host relationship involves different aspects such as the biochemical, physiological, morphological, and immunological adaptations. Studies on parasite-host interaction have provided a myriad of information about its biology and have established the building blocks for the development of new drug therapies to control the parasite. Several mechanisms for the parasite invasion have been proposed through in vivo or in vitro experimental data. Since the first histological studies until the studies on the function/structure of the involved molecules, this complex interaction has been roughly depicted. However, new recent strategies as genetic and proteomic approaches have tuned knowledge on how the host reacts to the parasite and how the parasite avoids these host's reactions in order to survive.

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Decreased cruzipain and gp85/trans-sialidase family protein expression contributes to loss of Trypanosoma cruzi trypomastigote virulence

Cited by 31 publications

References 33 publications

Trypanosoma cruzi Infection Induces Pannexin-1 Channel Opening in Cardiac Myocytes

Trypanosoma cruzi Infection Induces Pannexin-1 Channel Opening in Cardiac Myocytes

How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes

Biochemical, Cellular, and Immunologic Aspects during Early Interaction between Trypanosoma cruzi and Host Cell

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