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BioMed Research International
Volume 2014 (2014), Article ID 439501, 12 pages
Research Article

Early Trypanosoma cruzi Infection Reprograms Human Epithelial Cells

1Unidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, Uruguay
2Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Montevideo 11300, Uruguay
3Sección Genética, Facultad de Ciencias, Universidad de la República, Montevideo 11400, Uruguay

Received 6 December 2013; Revised 27 February 2014; Accepted 27 February 2014; Published 9 April 2014

Academic Editor: Wanderley de Souza

Copyright © 2014 María Laura Chiribao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.