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dc.contributor.authorStaquicini, Daniela I. [UNIFESP]
dc.contributor.authorMartins, Rafael M. [UNIFESP]
dc.contributor.authorMacedo, Silene [UNIFESP]
dc.contributor.authorSasso, Gisela R. S. [UNIFESP]
dc.contributor.authorAtayde, Vanessa [UNIFESP]
dc.contributor.authorJuliano, Maria Aparecida [UNIFESP]
dc.contributor.authorYoshida, Nobuko [UNIFESP]
dc.date.accessioned2016-01-24T13:59:22Z
dc.date.available2016-01-24T13:59:22Z
dc.date.issued2010-03-01
dc.identifierhttp://dx.doi.org/10.1371/journal.pntd.0000613
dc.identifier.citationPlos Neglected Tropical Diseases. San Francisco: Public Library Science, v. 4, n. 3, 9 p., 2010.
dc.identifier.issn1935-2727
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/32303
dc.description.abstractOral infection by Trypanosoma cruzi has been the primary cause of recent outbreaks of acute Chagas' diseases. This route of infection may involve selective binding of the metacyclic trypomastigote surface molecule gp82 to gastric mucin as a first step towards invasion of the gastric mucosal epithelium and subsequent systemic infection. Here we addressed that question by performing in vitro and in vivo experiments. A recombinant protein containing the complete gp82 sequence (J18), a construct lacking the gp82 central domain (J18*), and 20-mer synthetic peptides based on the gp82 central domain, were used for gastric mucin binding and HeLa cell invasion assays, or for in vivo experiments. Metacyclic trypomastigotes and J18 bound to gastric mucin whereas J18* failed to bind. Parasite or J18 binding to submaxillary mucin was negligible. HeLa cell invasion by metacyclic forms was not affected by gastric mucin but was inhibited in the presence of submaxillary mucin. of peptides tested for inhibition of J18 binding to gastric mucin, the inhibitory peptide p7 markedly reduced parasite invasion of HeLa cells in the presence of gastric mucin. Peptide p7*, with the same composition as p7 but with a scrambled sequence, had no effect. Mice fed with peptide p7 before oral infection with metacyclic forms developed lower parasitemias than mice fed with peptide p7*. Our results indicate that selective binding of gp82 to gastric mucin may direct T. cruzi metacyclic trypomastigotes to stomach mucosal epithelium in oral infection.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent9
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos Neglected Tropical Diseases
dc.rightsAcesso aberto
dc.titleRole of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzien
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionYale Univ
dc.description.affiliationUniversidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Morfol, São Paulo, Brazil
dc.description.affiliationYale Univ, Sch Med, Dept Internal Med & Cell Biol, New Haven, CT USA
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biofis, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Morfol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biofis, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 2006/61450-0
dc.description.sponsorshipIDCNPq: 470726/2007-5
dc.identifier.fileWOS000276312200029.pdf
dc.identifier.doi10.1371/journal.pntd.0000613
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000276312200029


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