Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/30237 http://dx.doi.org/10.1128/IAI.01199-07 |
Resumo: | Typical enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) employ either Nck, TccP/TccP2, or Nck and TccP/TccP2 pathways to activate the neuronal Wiskott-Aldrich syndrome protein (N-WASP) and to trigger actin polymerization in. cultured cells. This phenotype is used as a marker for the pathogenic potential of EPEC and EHEC strains. in this paper we report that EPEC O125:H6, which represents a large category of strains, lacks the ability to utilize either Nck or TccP/TccP2 and hence triggers actin polymerization in vitro only inefficiently. However, we show that infection of human intestinal biopsies with EPEC O125:H6 results in formation of typical attaching and effacing lesions. Expression of TccP in EPEC O125:H6, which harbors an EHEC O157-like Tir, resulted in efficient actin polymerization in vitro and enhanced colonization of human intestinal in vitro organ cultures with detectable N-WASP and electron-dense material at the site of bacterial adhesion. These results show the existence of a natural category of EPEC that colonizes the gut mucosa using Nck- and TccP-independent mechanisms. Importantly, the results highlight yet again the fact that conclusions made on the basis of in vitro cell culture models cannot be extrapolated wholesale to infection of mucosal surfaces and that the ability to induce actin polymerization on cultured cells should not be used as a definitive marker for EPEC and EHEC virulence. |
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Bai, LiSchuller, StephanieWhale, AndrewMousnier, AurelieMarches, OlivierWang, LeiOoka, TadasukeHeuschkel, RobertTorrente, FrancoKaper, James B.Gomes, Tania A. T. [UNIFESP]Xu, JianguoPhillips, Alan D.Frankel, GadUniv London Imperial Coll Sci Technol & MedChina CDCUCL Royal Free Univ Coll Med SchMiyazaki UnivUniv MarylandUniversidade Federal de São Paulo (UNIFESP)2016-01-24T13:49:19Z2016-01-24T13:49:19Z2008-01-01Infection and Immunity. Washington: Amer Soc Microbiology, v. 76, n. 1, p. 361-368, 2008.0019-9567http://repositorio.unifesp.br/handle/11600/30237http://dx.doi.org/10.1128/IAI.01199-07WOS000252126000039.pdf10.1128/IAI.01199-07WOS:000252126000039Typical enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) employ either Nck, TccP/TccP2, or Nck and TccP/TccP2 pathways to activate the neuronal Wiskott-Aldrich syndrome protein (N-WASP) and to trigger actin polymerization in. cultured cells. This phenotype is used as a marker for the pathogenic potential of EPEC and EHEC strains. in this paper we report that EPEC O125:H6, which represents a large category of strains, lacks the ability to utilize either Nck or TccP/TccP2 and hence triggers actin polymerization in vitro only inefficiently. However, we show that infection of human intestinal biopsies with EPEC O125:H6 results in formation of typical attaching and effacing lesions. Expression of TccP in EPEC O125:H6, which harbors an EHEC O157-like Tir, resulted in efficient actin polymerization in vitro and enhanced colonization of human intestinal in vitro organ cultures with detectable N-WASP and electron-dense material at the site of bacterial adhesion. These results show the existence of a natural category of EPEC that colonizes the gut mucosa using Nck- and TccP-independent mechanisms. Importantly, the results highlight yet again the fact that conclusions made on the basis of in vitro cell culture models cannot be extrapolated wholesale to infection of mucosal surfaces and that the ability to induce actin polymerization on cultured cells should not be used as a definitive marker for EPEC and EHEC virulence.Univ London Imperial Coll Sci Technol & Med, Div Cell & Mol Biol, London SW7 2AZ, EnglandChina CDC, Natl Inst Communicable Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Beijing, Peoples R ChinaUCL Royal Free Univ Coll Med Sch, Ctr Paediat Gastroenterol, London, EnglandMiyazaki Univ, Frontier Sci Res Ctr, Div Bioenvironm Sci, Miyazaki 8891692, JapanUniv Maryland, Sch Med, Ctr Vaccine Dev, Baltimore, MD 21201 USAUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilWeb of Science361-368engAmer Soc MicrobiologyInfection and ImmunityEnteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000252126000039.pdfapplication/pdf757915${dspace.ui.url}/bitstream/11600/30237/1/WOS000252126000039.pdfa111db0591280d49d19d54b2cf5624f8MD51open accessTEXTWOS000252126000039.pdf.txtWOS000252126000039.pdf.txtExtracted texttext/plain40232${dspace.ui.url}/bitstream/11600/30237/2/WOS000252126000039.pdf.txt101c38c755c40b15e8583a40ed8c4775MD52open access11600/302372022-09-27 09:38:19.002open accessoai:repositorio.unifesp.br:11600/30237Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T12:38:19Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
title |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
spellingShingle |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 Bai, Li |
title_short |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
title_full |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
title_fullStr |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
title_full_unstemmed |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
title_sort |
Enteropathogenic Escherichia coli O125 : H6 triggers attaching and effacing lesions on human intestinal biopsy specimens independently of nck and TccP/TccP2 |
author |
Bai, Li |
author_facet |
Bai, Li Schuller, Stephanie Whale, Andrew Mousnier, Aurelie Marches, Olivier Wang, Lei Ooka, Tadasuke Heuschkel, Robert Torrente, Franco Kaper, James B. Gomes, Tania A. T. [UNIFESP] Xu, Jianguo Phillips, Alan D. Frankel, Gad |
author_role |
author |
author2 |
Schuller, Stephanie Whale, Andrew Mousnier, Aurelie Marches, Olivier Wang, Lei Ooka, Tadasuke Heuschkel, Robert Torrente, Franco Kaper, James B. Gomes, Tania A. T. [UNIFESP] Xu, Jianguo Phillips, Alan D. Frankel, Gad |
author2_role |
author author author author author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Univ London Imperial Coll Sci Technol & Med China CDC UCL Royal Free Univ Coll Med Sch Miyazaki Univ Univ Maryland Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Bai, Li Schuller, Stephanie Whale, Andrew Mousnier, Aurelie Marches, Olivier Wang, Lei Ooka, Tadasuke Heuschkel, Robert Torrente, Franco Kaper, James B. Gomes, Tania A. T. [UNIFESP] Xu, Jianguo Phillips, Alan D. Frankel, Gad |
description |
Typical enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) employ either Nck, TccP/TccP2, or Nck and TccP/TccP2 pathways to activate the neuronal Wiskott-Aldrich syndrome protein (N-WASP) and to trigger actin polymerization in. cultured cells. This phenotype is used as a marker for the pathogenic potential of EPEC and EHEC strains. in this paper we report that EPEC O125:H6, which represents a large category of strains, lacks the ability to utilize either Nck or TccP/TccP2 and hence triggers actin polymerization in vitro only inefficiently. However, we show that infection of human intestinal biopsies with EPEC O125:H6 results in formation of typical attaching and effacing lesions. Expression of TccP in EPEC O125:H6, which harbors an EHEC O157-like Tir, resulted in efficient actin polymerization in vitro and enhanced colonization of human intestinal in vitro organ cultures with detectable N-WASP and electron-dense material at the site of bacterial adhesion. These results show the existence of a natural category of EPEC that colonizes the gut mucosa using Nck- and TccP-independent mechanisms. Importantly, the results highlight yet again the fact that conclusions made on the basis of in vitro cell culture models cannot be extrapolated wholesale to infection of mucosal surfaces and that the ability to induce actin polymerization on cultured cells should not be used as a definitive marker for EPEC and EHEC virulence. |
publishDate |
2008 |
dc.date.issued.fl_str_mv |
2008-01-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T13:49:19Z |
dc.date.available.fl_str_mv |
2016-01-24T13:49:19Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Infection and Immunity. Washington: Amer Soc Microbiology, v. 76, n. 1, p. 361-368, 2008. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/30237 http://dx.doi.org/10.1128/IAI.01199-07 |
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0019-9567 |
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WOS000252126000039.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1128/IAI.01199-07 |
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WOS:000252126000039 |
identifier_str_mv |
Infection and Immunity. Washington: Amer Soc Microbiology, v. 76, n. 1, p. 361-368, 2008. 0019-9567 WOS000252126000039.pdf 10.1128/IAI.01199-07 WOS:000252126000039 |
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http://repositorio.unifesp.br/handle/11600/30237 http://dx.doi.org/10.1128/IAI.01199-07 |
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eng |
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Amer Soc Microbiology |
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Amer Soc Microbiology |
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