Interaction with host factors exacerbates Trypanosoma cruzi cell invasion capacity upon oral infection

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dc.contributor.authorCovarrubias, Charles
dc.contributor.authorCortez, Mauro
dc.contributor.authorFerreira, Daniele
dc.contributor.authorYoshida, Nobuko
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:49:15Z
dc.date.available2016-01-24T13:49:15Z
dc.date.issued2007-12-01
dc.description.abstractOutbreaks of severe acute Chagas' disease acquired by oral infection, leading to death in some cases, have occurred in recent years. Using the mouse model, we investigated the basis of such virulence by analyzing a Trypanosoma cruzi isolate, SC, from a patient with severe acute clinical symptoms, who was infected by oral route. It has previously been shown that, upon oral inoculation into mice, T. cruzi metacyclic trypomastigotes invade the gastric mucosal epithelium by engaging the stage-specific surface glycoprotein gp82, whereas the surface molecule gp90 functions as a down-modulator of cell invasion. We found that, when orally inoculated into mice, metacyclic forms of the SC isolate, which express high levels of gp90, produced high parasitemias and high mortality, in sharp contrast with the reduced infectivity in vitro. Upon recovery from the mouse stomach I h after oral inoculation, the gp90 molecule of the parasites was completely degraded, and their entry into HeLa cells, as well as into Caco-2 cells, was increased. the gp82 molecule was more resistant to digestive action of the gastric juice. Host cell invasion of SC isolate metacyclic trypomastigotes was augmented in the presence of gastric mucin. No alteration in infectivity was observed in T. cruzi strains CL and G which were used as references and which express gp90 molecules resistant to degradation by gastric juice. Taken together, our findings suggest that the exacerbation of T. cruzi infectivity, such as observed upon interaction of the SC isolate with the mouse stomach components, may be responsible for the severity of acute Chagas' disease that has been reported in outbreaks of oral T. cruzi infection. (C) 2007 Australian Society for Parasitology Inc. Published by Elsevier B.V. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1609-1616
dc.identifierhttp://dx.doi.org/10.1016/j.ijpara.2007.05.013
dc.identifier.citationInternational Journal for Parasitology. Oxford: Pergamon-Elsevier B.V., v. 37, n. 14, p. 1609-1616, 2007.
dc.identifier.doi10.1016/j.ijpara.2007.05.013
dc.identifier.issn0020-7519
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30184
dc.identifier.wosWOS:000250900200008
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofInternational Journal for Parasitology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectTrypanosoma cruzien
dc.subjectoral infectionen
dc.subjectmetacyclic trypomastigotesen
dc.subjecthost factorsen
dc.subjectmodulation of infectivityen
dc.subjectcell invasionen
dc.titleInteraction with host factors exacerbates Trypanosoma cruzi cell invasion capacity upon oral infectionen
dc.typeinfo:eu-repo/semantics/article
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