Binding of Nicotinic Ligands to and Nicotine-Induced Calcium Signaling in Trypanosoma cruzi

2001 ◽  
Vol 281 (2) ◽  
pp. 300-304 ◽  
Author(s):  
Mariana Bollo ◽  
Graciela Venera ◽  
Mirtha Biscoglio de Jiménez Bonino ◽  
Estela Machado-Domenech
Keyword(s):  
Trypanosoma Cruzi ◽  
Calcium Signaling

scholarly journals Biological and Molecular Effects of Trypanosoma cruzi Residence in a LAMP-Deficient Intracellular Environment

2022 ◽  
Vol 11 ◽  
Author(s):  
Anny Carolline Silva Oliveira ◽  
Luisa Rezende ◽  
Vladimir Gorshkov ◽  
Marcella Nunes Melo-Braga ◽  
Thiago Verano-Braga ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Calcium Signaling ◽  
Surface Membrane ◽  
Host Cells ◽  
Biological Behavior ◽  
Membrane Repair ◽  
Phagocytic Cells ◽  
Membrane Injury ◽  
Injury Rates ◽  
Intracellular Environment

Trypanosoma cruzi invades non-professional phagocytic cells by subverting their membrane repair process, which is dependent on membrane injury and cell signaling, intracellular calcium increase, and lysosome recruitment. Cells lacking lysosome-associated membrane proteins 1 and 2 (LAMP1 and LAMP2) are less permissive to parasite invasion but more prone to parasite intracellular multiplication. Several passages through a different intracellular environment can significantly change T. cruzi’s gene expression profile. Here, we evaluated whether one single passage through LAMP-deficient (KO) or wild-type (WT) fibroblasts, thus different intracellular environments, could influence T. cruzi Y strain trypomastigotes’ ability to invade L6 myoblasts and WT fibroblasts host cells. Parasites released from LAMP2 KO cells (TcY-L2−/−) showed higher invasion, calcium signaling, and membrane injury rates, for the assays in L6 myoblasts, when compared to those released from WT (TcY-WT) or LAMP1/2 KO cells (TcY-L1/2−/−). On the other hand, TcY-L1/2−/− showed higher invasion, calcium signaling, and cell membrane injury rates, for the assays in WT fibroblasts, compared to TcY-WT and TcY-L1/2−/−. Albeit TcY-WT presented an intermediary invasion and calcium signaling rates, compared to the others, in WT fibroblasts, they induced lower levels of injury, which reinforces that signals mediated by surface membrane protein interactions also have a significant contribution to trigger host cell calcium signals. These results clearly show that parasites released from WT or LAMP KO cells are distinct from each other. Additionally, these parasites’ ability to invade the cell may be distinct depending on which cell type they interact with. Since these alterations most likely would reflect differences among parasite surface molecules, we also evaluated their proteome. We identified few protein complexes, membrane, and secreted proteins regulated in our dataset. Among those are some members of MASP, mucins, trans-sialidases, and gp63 proteins family, which are known to play an important role during parasite infection and could correlate to TcY-WT, TcY-L1/2−/−, and TcY-L2−/− biological behavior.

scholarly journals Interaction With the Extracellular Matrix Triggers Calcium Signaling in Trypanosoma cruzi Prior to Cell Invasion

2021 ◽  
Vol 11 ◽  
Author(s):  
Nubia Carolina Manchola Varón ◽  
Guilherme Rodrigo R. M. dos Santos ◽  
Walter Colli ◽  
Maria Julia M. Alves
Keyword(s):  
Extracellular Matrix ◽  
Tissue Culture ◽  
Plasma Membrane ◽  
Trypanosoma Cruzi ◽  
Calcium Signaling ◽  
Host Cell ◽  
Cell Invasion ◽  
Early Phase ◽  
Host Cell Invasion ◽  
Dependent Manner

Trypanosoma cruzi, the etiological agent of Chagas disease in humans, infects a wide variety of vertebrates. Trypomastigotes, the parasite infective forms, invade mammalian cells by a still poorly understood mechanism. Adhesion of tissue culture- derived trypomastigotes to the extracellular matrix (ECM) prior to cell invasion has been shown to be a relevant part of the process. Changes in phosphorylation, S-nitrosylation, and nitration levels of proteins, in the late phase of the interaction (2 h), leading to the reprogramming of both trypomastigotes metabolism and the DNA binding profile of modified histones, were described by our group. Here, the involvement of calcium signaling at a very early phase of parasite interaction with ECM is described. Increments in the intracellular calcium concentrations during trypomastigotes-ECM interaction depends on the Ca2+ uptake from the extracellular medium, since it is inhibited by EGTA or Nifedipine, an inhibitor of the L-type voltage gated Ca2+ channels and sphingosine-dependent plasma membrane Ca2+ channel, but not by Vanadate, an inhibitor of the plasma membrane Ca2+-ATPase. Furthermore, Nifedipine inhibits the invasion of host cells by tissue culture- derived trypomastigotes in a dose-dependent manner, reaching 95% inhibition at 100 µM Nifedipine. These data indicate the importance of both Ca2+ uptake from the medium and parasite-ECM interaction for host-cell invasion. Previous treatment of ECM with protease abolishes the Ca2+ uptake, further reinforcing the possibility that these events may be connected. The mitochondrion plays a relevant role in Ca2+ homeostasis in trypomastigotes during their interaction with ECM, as shown by the increment of the intracellular Ca2+ concentration in the presence of Antimycin A, in contrast to other calcium homeostasis disruptors, such as Cyclopiazonic acid for endoplasmic reticulum and Bafilomycin A for acidocalcisome. Total phosphatase activity in the parasite decreases in the presence of Nifedipine, EGTA, and Okadaic acid, implying a role of calcium in the phosphorylation level of proteins that are interacting with the ECM in tissue culture- derived trypomastigotes. In summary, we describe here the increment of Ca2+ at an early phase of the trypomastigotes interaction with ECM, implicating both nifedipine-sensitive Ca2+ channels in the influx of Ca2+ and the mitochondrion as the relevant organelle in Ca2+ homeostasis. The data unravel a complex sequence of events prior to host cell invasion itself.

Protective effect of Trypanosoma rangeli against infections with a highly virulent strain of Trypanosoma cruzi

1997 ◽  
Vol 2 (5) ◽  
pp. 482-487 ◽  
Author(s):  
Claudio Zuniga ◽  
Teresa Palau ◽  
Pilar Penin ◽  
Carlos Gamallo ◽  
Jose Antonio de Diego
Keyword(s):  
Trypanosoma Cruzi ◽  
Protective Effect ◽  
Virulent Strain ◽  
Trypanosoma Rangeli ◽  
Highly Virulent

Unusual dimeric flavonoids from Arrabidaea brachypoda with very significant in vitro and in vivo anti-Trypanosoma cruzi activity

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
C Quitino-da-Rocha ◽  
E Ferreira-Queiroz ◽  
C Santana-Meira ◽  
DR Magalhães-Moreira ◽  
M Botelho-Pereira-Soares ◽  
...  
Keyword(s):  
Trypanosoma Cruzi
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