Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans

Autores
Lachance, Claude; Segura, Mariela; Pereyra Gerber, Federico Pehuén; Xu, Jianguo; Gottschalk, Marcelo
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2−/−) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2−/− mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2−/− mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain.
Fil: Lachance, Claude. University of Montreal; Canadá
Fil: Segura, Mariela. University of Montreal; Canadá
Fil: Pereyra Gerber, Federico Pehuén. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Xu, Jianguo. Chinese Center for Disease Control and Prevention; China
Fil: Gottschalk, Marcelo. University of Montreal; Canadá
Materia
Streptococcus Suis
Toll-Like Receptor 2
Toxic-Shock Syndrome
Host Response to Pathogen
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/2537
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/2537
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in HumansLachance, ClaudeSegura, MarielaPereyra Gerber, Federico PehuénXu, JianguoGottschalk, MarceloStreptococcus SuisToll-Like Receptor 2Toxic-Shock SyndromeHost Response to Pathogenhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2−/−) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2−/− mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2−/− mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain.Fil: Lachance, Claude. University of Montreal; CanadáFil: Segura, Mariela. University of Montreal; CanadáFil: Pereyra Gerber, Federico Pehuén. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Xu, Jianguo. Chinese Center for Disease Control and Prevention; ChinaFil: Gottschalk, Marcelo. University of Montreal; CanadáPublic Library of Science2013-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/2537Lachance, Claude; Segura, Mariela; Pereyra Gerber, Federico Pehuén; Xu, Jianguo; Gottschalk, Marcelo; Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans; Public Library of Science; Plos One; 8; 5; 5-2013; e65031-e650311932-6203enginfo:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665724/info:eu-repo/semantics/altIdentifier/doi/10.1371%2Fjournal.pone.0065031info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0065031info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:41:31Zoai:ri.conicet.gov.ar:11336/2537instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:41:31.621CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
title Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
spellingShingle Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
Lachance, Claude
Streptococcus Suis
Toll-Like Receptor 2
Toxic-Shock Syndrome
Host Response to Pathogen
title_short Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
title_full Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
title_fullStr Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
title_full_unstemmed Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
title_sort Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans
dc.creator.none.fl_str_mv Lachance, Claude
Segura, Mariela
Pereyra Gerber, Federico Pehuén
Xu, Jianguo
Gottschalk, Marcelo
author Lachance, Claude
author_facet Lachance, Claude
Segura, Mariela
Pereyra Gerber, Federico Pehuén
Xu, Jianguo
Gottschalk, Marcelo
author_role author
author2 Segura, Mariela
Pereyra Gerber, Federico Pehuén
Xu, Jianguo
Gottschalk, Marcelo
author2_role author
author
author
author
dc.subject.none.fl_str_mv Streptococcus Suis
Toll-Like Receptor 2
Toxic-Shock Syndrome
Host Response to Pathogen
topic Streptococcus Suis
Toll-Like Receptor 2
Toxic-Shock Syndrome
Host Response to Pathogen
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2−/−) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2−/− mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2−/− mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain.
Fil: Lachance, Claude. University of Montreal; Canadá
Fil: Segura, Mariela. University of Montreal; Canadá
Fil: Pereyra Gerber, Federico Pehuén. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Xu, Jianguo. Chinese Center for Disease Control and Prevention; China
Fil: Gottschalk, Marcelo. University of Montreal; Canadá
description Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2−/−) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2−/− mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2−/− mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain.
publishDate 2013
dc.date.none.fl_str_mv 2013-05
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/2537
Lachance, Claude; Segura, Mariela; Pereyra Gerber, Federico Pehuén; Xu, Jianguo; Gottschalk, Marcelo; Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans; Public Library of Science; Plos One; 8; 5; 5-2013; e65031-e65031
1932-6203
url http://hdl.handle.net/11336/2537
identifier_str_mv Lachance, Claude; Segura, Mariela; Pereyra Gerber, Federico Pehuén; Xu, Jianguo; Gottschalk, Marcelo; Toll-Like Receptor 2-Independent Host Innate Immune Response against an Epidemic Strain of Streptococcus suis That Causes a Toxic Shock-Like Syndrome in Humans; Public Library of Science; Plos One; 8; 5; 5-2013; e65031-e65031
1932-6203
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665724/
info:eu-repo/semantics/altIdentifier/doi/10.1371%2Fjournal.pone.0065031
info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0065031
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.982451

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