Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells
Trypanosoma cruzi, the causative agent of Chagas disease, has the peculiarity, when compared with other intracellular parasites, that it is able to invade almost any type of cell. This property makes Chagas a complex parasitic disease in terms of prophylaxis and therapeutics. The identification of k...
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doaj-133a0f3e6e124fce996fdbb983f4e2ae2020-11-24T21:36:26ZengHindawi LimitedBioMed Research International2314-61332314-61412014-01-01201410.1155/2014/439501439501Early Trypanosoma cruzi Infection Reprograms Human Epithelial CellsMaría Laura Chiribao0Gabriela Libisch1Adriana Parodi-Talice2Carlos Robello3Unidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, UruguayUnidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, UruguayUnidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, UruguayUnidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, UruguayTrypanosoma cruzi, the causative agent of Chagas disease, has the peculiarity, when compared with other intracellular parasites, that it is able to invade almost any type of cell. This property makes Chagas a complex parasitic disease in terms of prophylaxis and therapeutics. The identification of key host cellular factors that play a role in the T. cruzi invasion is important for the understanding of disease pathogenesis. In Chagas disease, most of the focus is on the response of macrophages and cardiomyocytes, since they are responsible for host defenses and cardiac lesions, respectively. In the present work, we studied the early response to infection of T. cruzi in human epithelial cells, which constitute the first barrier for establishment of infection. These studies identified up to 1700 significantly altered genes regulated by the immediate infection. The global analysis indicates that cells are literally reprogrammed by T. cruzi, which affects cellular stress responses (neutrophil chemotaxis, DNA damage response), a great number of transcription factors (including the majority of NFκB family members), and host metabolism (cholesterol, fatty acids, and phospholipids). These results raise the possibility that early host cell reprogramming is exploited by the parasite to establish the initial infection and posterior systemic dissemination.http://dx.doi.org/10.1155/2014/439501 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
María Laura Chiribao Gabriela Libisch Adriana Parodi-Talice Carlos Robello |
spellingShingle |
María Laura Chiribao Gabriela Libisch Adriana Parodi-Talice Carlos Robello Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells BioMed Research International |
author_facet |
María Laura Chiribao Gabriela Libisch Adriana Parodi-Talice Carlos Robello |
author_sort |
María Laura Chiribao |
title |
Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells |
title_short |
Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells |
title_full |
Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells |
title_fullStr |
Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells |
title_full_unstemmed |
Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells |
title_sort |
early trypanosoma cruzi infection reprograms human epithelial cells |
publisher |
Hindawi Limited |
series |
BioMed Research International |
issn |
2314-6133 2314-6141 |
publishDate |
2014-01-01 |
description |
Trypanosoma cruzi, the causative agent of Chagas disease, has the peculiarity, when compared with other intracellular parasites, that it is able to invade almost any type of cell. This property makes Chagas a complex parasitic disease in terms of prophylaxis and therapeutics. The identification of key host cellular factors that play a role in the T. cruzi invasion is important for the understanding of disease pathogenesis. In Chagas disease, most of the focus is on the response of macrophages and cardiomyocytes, since they are responsible for host defenses and cardiac lesions, respectively. In the present work, we studied the early response to infection of T. cruzi in human epithelial cells, which constitute the first barrier for establishment of infection. These studies identified up to 1700 significantly altered genes regulated by the immediate infection. The global analysis indicates that cells are literally reprogrammed by T. cruzi, which affects cellular stress responses (neutrophil chemotaxis, DNA damage response), a great number of transcription factors (including the majority of NFκB family members), and host metabolism (cholesterol, fatty acids, and phospholipids). These results raise the possibility that early host cell reprogramming is exploited by the parasite to establish the initial infection and posterior systemic dissemination. |
url |
http://dx.doi.org/10.1155/2014/439501 |
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