Trypanosoma cruzi Infection through the Oral Route Promotes a Severe Infection in Mice: New Disease Form from an Old Infection?

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dc.creator Barreto-de-Albuquerque, Juliana
dc.creator Silva-dos-Santos, Danielle
dc.creator Pérez, Ana Rosa
dc.creator Berbert, Luiz Ricardo
dc.creator de Santana-van-Vliet, Eliane
dc.creator Farias-de-Oliveira, Désio Aurélio
dc.creator Moreira, Otacilio C.
dc.creator Roggero, Eduardo
dc.creator de Carvalho-Pinto, Carla Eponina
dc.creator Jurberg, José
dc.creator Cotta-de-Almeida, Vinícius
dc.creator Bottasso, Oscar
dc.creator Savino, Wilson
dc.creator de Meis, Juliana
dc.date.accessioned 2015-08-13T13:26:45Z
dc.date.available 2015-08-13T13:26:45Z
dc.date.issued 2015-06-19
dc.identifier.issn 1935-2735 es
dc.identifier.uri http://hdl.handle.net/2133/4879
dc.description Oral transmission of Chagas disease has been documented in Latin American countries. Nevertheless, significant studies on the pathophysiology of this form of infection are largely lacking. The few studies investigating oral route infection disregard that inoculation in the oral cavity (Oral infection, OI) or by gavage (Gastrointestinal infection, GI) represent different infection routes, yet both show clear-cut parasitemia and heart parasitism during the acute infection. Herein, BALB/c mice were subjected to acute OI or GI infection using 5x104 culture-derived Trypanosoma cruzi trypomastigotes. OI mice displayed higher parasitemia and mortality rates than their GI counterparts. Heart histopathology showed larger areas of infiltration in the GI mice, whereas liver lesions were more severe in the OI animals, accompanied by higher Alanine Transaminase and Aspartate Transaminase serum contents. A differential cytokine pattern was also observed because OI mice presented higher pro-inflammatory cytokine (IFN-γ, TNF) serum levels than GI animals. Real-time PCR confirmed a higher TNF, IFN-γ, as well as IL-10 expression in the cardiac tissue from the OI group compared with GI. Conversely, TGF-β and IL-17 serum levels were greater in the GI animals. Immunolabeling revealed macrophages as the main tissue source of TNF in infected mice. The high mortality rate observed in the OI mice paralleled the TNF serum rise, with its inhibition by an anti-TNF treatment. Moreover, differences in susceptibility between GI versus OI mice were more clearly related to the host response than to the effect of gastric pH on parasites, since infection in magnesium hydroxide-treated mice showed similar results. Overall, the present study provides conclusive evidence that the initial site of parasite entrance critically affects host immune response and disease outcome. In light of the occurrence of oral Chagas disease outbreaks, our results raise important implications in terms of the current view of the natural disease course and host-parasite relationship. es
dc.description.sponsorship This work was supported by the Rio de Janeiro State Research Foundation (FAPERJ-Grant E-26/103.249/2011) and Brazilian National Research Council (CNPq-Grant 479431/2011-6) to JdM. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. es
dc.format application/pdf
dc.format.extent 1-21 es
dc.language.iso eng es
dc.publisher PLOS (Public Library of Science) es
dc.rights openAccess es
dc.rights.uri http://creativecommons.org/licenses/by/4.0/ *
dc.source PLOS Neglected Tropical Diseases es
dc.subject Genitourinary infections es
dc.subject Parasitic diseases es
dc.subject Trypanosoma cruzi es
dc.subject Gastrointestinal infections es
dc.subject Heart es
dc.subject Trypomastigotes es
dc.subject Parasitemia es
dc.title Trypanosoma cruzi Infection through the Oral Route Promotes a Severe Infection in Mice: New Disease Form from an Old Infection? es
dc.type article
dc.type artículo
dc.type publishedVersion
dc.rights.holder © 2015 Barreto-de-Albuquerque et al. es
dc.relation.publisherversion doi:10.1371/journal.pntd.0003849 es
dc.rights.text This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. es
dc.citation.title PLOS Neglected Tropical Diseases es
dc.citation.volume PLoS Negl Trop Dis 9(6): e0003849 es
dc.description.fil Fil: Pérez, Ana Rosa. Immunology Institute, Faculty of Medical Science, National University of Rosario, Rosario, Argentina es
dc.description.fil Fil: Roggero, Eduardo. Immunology Institute, Faculty of Medical Science, National University of Rosario, Rosario, Argentina es
dc.description.fil Fil: Bottasso, Oscar. Immunology Institute, Faculty of Medical Science, National University of Rosario, Rosario, Argentina es
dc.type.collection articulo


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