Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi
Autor(a) principal: | |
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Data de Publicação: | 2010 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/32303 http://dx.doi.org/10.1371/journal.pntd.0000613 |
Resumo: | Oral 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. |
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Staquicini, Daniela I. [UNIFESP]Martins, Rafael M. [UNIFESP]Macedo, Silene [UNIFESP]Sasso, Gisela R. S. [UNIFESP]Atayde, Vanessa [UNIFESP]Juliano, Maria Aparecida [UNIFESP]Yoshida, Nobuko [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Yale Univ2016-01-24T13:59:22Z2016-01-24T13:59:22Z2010-03-01Plos Neglected Tropical Diseases. San Francisco: Public Library Science, v. 4, n. 3, 9 p., 2010.1935-2727http://repositorio.unifesp.br/handle/11600/32303http://dx.doi.org/10.1371/journal.pntd.0000613WOS000276312200029.pdf10.1371/journal.pntd.0000613WOS:000276312200029Oral 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.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Morfol, São Paulo, BrazilYale Univ, Sch Med, Dept Internal Med & Cell Biol, New Haven, CT USAUniversidade Federal de São Paulo, Dept Biofis, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Morfol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biofis, São Paulo, BrazilFAPESP: 2006/61450-0CNPq: 470726/2007-5Web of Science9engPublic Library SciencePlos Neglected Tropical DiseasesRole of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruziinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000276312200029.pdfapplication/pdf918242${dspace.ui.url}/bitstream/11600/32303/1/WOS000276312200029.pdfd2a447f725e16d10c1c2c024a61fa78bMD51open accessTEXTWOS000276312200029.pdf.txtWOS000276312200029.pdf.txtExtracted texttext/plain41555${dspace.ui.url}/bitstream/11600/32303/2/WOS000276312200029.pdf.txt7148c57c271c07eb45cd3773e4cf9278MD52open access11600/323032022-11-04 14:18:44.897open accessoai:repositorio.unifesp.br:11600/32303Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-11-04T17:18:44Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
title |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
spellingShingle |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi Staquicini, Daniela I. [UNIFESP] |
title_short |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
title_full |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
title_fullStr |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
title_full_unstemmed |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
title_sort |
Role of GP82 in the Selective Binding to Gastric Mucin during Oral Infection with Trypanosoma cruzi |
author |
Staquicini, Daniela I. [UNIFESP] |
author_facet |
Staquicini, Daniela I. [UNIFESP] Martins, Rafael M. [UNIFESP] Macedo, Silene [UNIFESP] Sasso, Gisela R. S. [UNIFESP] Atayde, Vanessa [UNIFESP] Juliano, Maria Aparecida [UNIFESP] Yoshida, Nobuko [UNIFESP] |
author_role |
author |
author2 |
Martins, Rafael M. [UNIFESP] Macedo, Silene [UNIFESP] Sasso, Gisela R. S. [UNIFESP] Atayde, Vanessa [UNIFESP] Juliano, Maria Aparecida [UNIFESP] Yoshida, Nobuko [UNIFESP] |
author2_role |
author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Yale Univ |
dc.contributor.author.fl_str_mv |
Staquicini, Daniela I. [UNIFESP] Martins, Rafael M. [UNIFESP] Macedo, Silene [UNIFESP] Sasso, Gisela R. S. [UNIFESP] Atayde, Vanessa [UNIFESP] Juliano, Maria Aparecida [UNIFESP] Yoshida, Nobuko [UNIFESP] |
description |
Oral 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. |
publishDate |
2010 |
dc.date.issued.fl_str_mv |
2010-03-01 |
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2016-01-24T13:59:22Z |
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2016-01-24T13:59:22Z |
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info:eu-repo/semantics/publishedVersion |
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dc.identifier.citation.fl_str_mv |
Plos Neglected Tropical Diseases. San Francisco: Public Library Science, v. 4, n. 3, 9 p., 2010. |
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http://repositorio.unifesp.br/handle/11600/32303 http://dx.doi.org/10.1371/journal.pntd.0000613 |
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1935-2727 |
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WOS000276312200029.pdf |
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Plos Neglected Tropical Diseases. San Francisco: Public Library Science, v. 4, n. 3, 9 p., 2010. 1935-2727 WOS000276312200029.pdf 10.1371/journal.pntd.0000613 WOS:000276312200029 |
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