Role of membrane N-linked oligosaccharides in host cell interaction with invasive forms of Trypanosoma cruzi

1987 ◽  
Vol 22 (2-3) ◽  
pp. 109-114 ◽  
Author(s):  
Fernando Villalta ◽  
Felipe Kierszenbaum
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Interaction ◽  
Host Cell Interaction

scholarly journals Improved enzyme-linked immunoadsorbent assay (ELISA) for the study of Trypanosoma cruzi-host cell interaction in vitro

1993 ◽  
Vol 88 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Mauricio R. M. P. Luz ◽  
Maria de Nazaré C. Soeiro ◽  
Tania C. Araújo-Jorge
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Interaction ◽  
Host Cell Interaction

scholarly journals Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

2019 ◽  
Vol 20 (19) ◽  
pp. 4836
Author(s):  
Tatiana Araújo Silva ◽  
Luis Felipe de Carvalho Ferreira ◽  
Mirian Claudia de Souza Pereira ◽  
Claudia Magalhães Calvet
Keyword(s):  
Trypanosoma Cruzi ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Cell Interaction ◽  
Skeletal Myoblasts ◽  
Growth Factor Beta ◽  
Cruzi Infection ◽  
Host Cell Interaction

Transforming growth factor beta (TGF-β) is a determinant for inflammation and fibrosis in cardiac and skeletal muscle in Chagas disease. To determine its regulatory mechanisms, we investigated the response of Trypanosoma cruzi-infected cardiomyocytes (CM), cardiac fibroblasts (CF), and L6E9 skeletal myoblasts to TGF-β. Cultures of CM, CF, and L6E9 were infected with T. cruzi (Y strain) and treated with TGF-β (1–10 ng/mL, 1 h or 48 h). Fibronectin (FN) distribution was analyzed by immunofluorescence and Western blot (WB). Phosphorylated SMAD2 (PS2), phospho-p38 (p-p38), and phospho-c-Jun (p-c-Jun) signaling were evaluated by WB. CF and L6E9 showed an increase in FN from 1 ng/mL of TGF-β, while CM displayed FN modulation only after 10 ng/mL treatment. CF and L6E9 showed higher PS2 levels than CM, while p38 was less stimulated in CF than CM and L6E9. T. cruzi infection resulted in localized FN disorganization in CF and L6E9. T. cruzi induced an increase in FN in CF cultures, mainly in uninfected cells. Infected CF cultures treated with TGF-β showed a reduction in PS2 and an increase in p-p38 and p-c-Jun levels. Our data suggest that p38 and c-Jun pathways may be participating in the fibrosis regulatory process mediated by TGF-β after T. cruzi infection.

scholarly journals Cysteine proteinase in Trypanosoma cruzi: immunocytochemical localization and involvement in parasite-host cell interaction

1990 ◽  
Vol 96 (3) ◽  
pp. 485-490
Author(s):  
T. Souto-Padron ◽  
O.E. Campetella ◽  
J.J. Cazzulo ◽  
W. de Souza
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cysteine Proteinase ◽  
Cell Interaction ◽  
Immunocytochemical Localization ◽  
Flagellar Pocket ◽  
Surface Localization ◽  
Axenic Cultures ◽  
Cytoplasmic Structures ◽  
Host Cell Interaction

A monospecific polyclonal antibody obtained against a cysteine proteinase isolated from epimastigotes of Trypanosoma cruzi was used for the immunocytochemical localization of the protein by electron microscopy and to analyse the role played by cysteine proteinase in the process of T. cruzi-host cell interaction. Cytoplasmic structures that correspond to elements of the endosomal-lysosomal (reservosome) system found in epimastigote, amastigote and trypomastigote forms reacted intensely with colloidal gold-labelled antibodies using on-section indirect labelling. The surface of most of the tissue culture-derived trypomastigotes was not labelled. However, the flagellar pocket of this form was labelled. All epimastigotes obtained from axenic cultures and amastigote-like forms found in the supernatant of vertebrate cells heavily infected with T. cruzi had their surface intensely labelled, indicating also the surface localization of the protein. Incubation of the parasites in the presence of a sub-agglutinating concentration of the anti-cysteine proteinase antibody led to a marked increase in their uptake by macrophages. In contrast, addition of the F(ab')2 portion of the same antibody significantly reduced the uptake of the parasites by the macrophages. The results obtained strongly suggest an important participation of cysteine proteinase in the process of T. cruzi-macrophage interaction.

Ecto-ATPase activity on the surface of Trypanosoma cruzi and its possible role in the parasite?host cell interaction

2003 ◽  
Vol 91 (4) ◽  
pp. 273-282 ◽  
Author(s):  
Danielle F. R. Bisaggio ◽  
Carlos Eduardo Peres-Sampaio ◽  
Jos� Roberto Meyer-Fernandes ◽  
Tha�s Souto-Padr�n
Keyword(s):  
Trypanosoma Cruzi ◽  
Atpase Activity ◽  
Host Cell ◽  
Cell Interaction ◽  
Host Cell Interaction

scholarly journals Hazara virus and Crimean-Congo Hemorrhagic Fever Virus show a different pattern of entry in fully-polarized Caco-2 cell line

2020 ◽  
Vol 14 (11) ◽  
pp. e0008863
Author(s):  
Vanessa Monteil ◽  
Cristiano Salata ◽  
Sofia Appelberg ◽  
Ali Mirazimi
Keyword(s):  
Host Cell ◽  
Cell Line ◽  
Hemorrhagic Fever ◽  
Cell Interaction ◽  
Fever Virus ◽  
Inflammatory Factors ◽  
Crimean Congo Hemorrhagic Fever ◽  
Hemorrhagic Fever Virus ◽  
Host Cell Interaction

Crimean-Congo Hemorrhagic Fever Virus (CCHFV) and Hazara virus (HAZV) belong to the same viral serotype and family. HAZV has lately been used as a model system and surrogate to CCHFV. However, virus-host cell interaction and level of pathogenicity for these viruses are not well investigated nor compared. In this study, we compared HAZV and CCHFV infection of human polarized epithelial cells to shed light on similarities and differences in virus-host cell interaction between these two viruses. We investigated the pattern of infection of CCHFV and HAZV in fully polarized human cells, the Caco-2 cell line. Polarization of Caco-2 cells lead to difference in expression level and pattern of proteins between the apical and the basolateral membranes. We found that CCHFV virus, in contrast to HAZV, is more likely infecting polarized cells basolaterally. In addition, we found that cytokines/pro-inflammatory factors or other viral factors secreted from CCHFV infected moDC cells enhance the entry of CCHFV contrary to HAZV. We have shown that CCHFV and HAZV early in infection use different strategies for entry. The data presented in this study also highlight the important role of cytokines in CCHFV-host cell interaction.

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