Bordetella pertussis modulates human macrophage defense gene expression
- Autores
- Valdez, Hugo Alberto; Oviedo, Juan Marcos; Gorgojo, Juan Pablo; Lamberti, Yanina Andrea; Rodríguez, María Eugenia
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Bordetella pertussis, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that B. pertussis can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In this work, we examined the interaction of B. pertussis with a human monocyte cell line (THP-1) that differentiates into macrophages in culture in order to investigate the host cell response to the infection and the mechanisms that promote that intracellular survival. To that end, we investigated the expression profile of a selected number of genes involved in cellular bactericidal activity and the inflammatory response during the early and late phases of infection. The bactericidal and inflammatory response of infected macrophages was progressively downregulated, while the number of THP-1 cells heavily loaded with live bacteria increased over time postinfection. Two of the main toxins of B. pertussis, pertussis toxin (Ptx) and adenylate cyclase (CyaA), were found to be involved in manipulating the host cell response. Therefore, failure to express either toxin proved detrimental to the development of intracellular infections by those bacteria. Taken together, these results support the relevance of host defense gene manipulation to the outcome of the interaction between B. pertussis and macrophages.
Facultad de Ciencias Exactas
Centro de Investigación y Desarrollo en Fermentaciones Industriales - Materia
-
Ciencias Exactas
Adenylate cyclase
Bordetella pertussis
Host cell defense response
Intracellular survival
Pertussis toxin - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/85803
Ver los metadatos del registro completo
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Bordetella pertussis modulates human macrophage defense gene expressionValdez, Hugo AlbertoOviedo, Juan MarcosGorgojo, Juan PabloLamberti, Yanina AndreaRodríguez, María EugeniaCiencias ExactasAdenylate cyclaseBordetella pertussisHost cell defense responseIntracellular survivalPertussis toxin<i>Bordetella pertussis</i>, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that <i>B. pertussis</i> can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In this work, we examined the interaction of <i>B. pertussis</i> with a human monocyte cell line (THP-1) that differentiates into macrophages in culture in order to investigate the host cell response to the infection and the mechanisms that promote that intracellular survival. To that end, we investigated the expression profile of a selected number of genes involved in cellular bactericidal activity and the inflammatory response during the early and late phases of infection. The bactericidal and inflammatory response of infected macrophages was progressively downregulated, while the number of THP-1 cells heavily loaded with live bacteria increased over time postinfection. Two of the main toxins of <i>B. pertussis</i>, pertussis toxin (Ptx) and adenylate cyclase (CyaA), were found to be involved in manipulating the host cell response. Therefore, failure to express either toxin proved detrimental to the development of intracellular infections by those bacteria. Taken together, these results support the relevance of host defense gene manipulation to the outcome of the interaction between <i>B. pertussis</i> and macrophages.Facultad de Ciencias ExactasCentro de Investigación y Desarrollo en Fermentaciones Industriales2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/85803enginfo:eu-repo/semantics/altIdentifier/issn/2049-632Xinfo:eu-repo/semantics/altIdentifier/doi/10.1093/femspd/ftw073info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:16:45Zoai:sedici.unlp.edu.ar:10915/85803Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:16:45.362SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Bordetella pertussis modulates human macrophage defense gene expression |
title |
Bordetella pertussis modulates human macrophage defense gene expression |
spellingShingle |
Bordetella pertussis modulates human macrophage defense gene expression Valdez, Hugo Alberto Ciencias Exactas Adenylate cyclase Bordetella pertussis Host cell defense response Intracellular survival Pertussis toxin |
title_short |
Bordetella pertussis modulates human macrophage defense gene expression |
title_full |
Bordetella pertussis modulates human macrophage defense gene expression |
title_fullStr |
Bordetella pertussis modulates human macrophage defense gene expression |
title_full_unstemmed |
Bordetella pertussis modulates human macrophage defense gene expression |
title_sort |
Bordetella pertussis modulates human macrophage defense gene expression |
dc.creator.none.fl_str_mv |
Valdez, Hugo Alberto Oviedo, Juan Marcos Gorgojo, Juan Pablo Lamberti, Yanina Andrea Rodríguez, María Eugenia |
author |
Valdez, Hugo Alberto |
author_facet |
Valdez, Hugo Alberto Oviedo, Juan Marcos Gorgojo, Juan Pablo Lamberti, Yanina Andrea Rodríguez, María Eugenia |
author_role |
author |
author2 |
Oviedo, Juan Marcos Gorgojo, Juan Pablo Lamberti, Yanina Andrea Rodríguez, María Eugenia |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
Ciencias Exactas Adenylate cyclase Bordetella pertussis Host cell defense response Intracellular survival Pertussis toxin |
topic |
Ciencias Exactas Adenylate cyclase Bordetella pertussis Host cell defense response Intracellular survival Pertussis toxin |
dc.description.none.fl_txt_mv |
<i>Bordetella pertussis</i>, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that <i>B. pertussis</i> can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In this work, we examined the interaction of <i>B. pertussis</i> with a human monocyte cell line (THP-1) that differentiates into macrophages in culture in order to investigate the host cell response to the infection and the mechanisms that promote that intracellular survival. To that end, we investigated the expression profile of a selected number of genes involved in cellular bactericidal activity and the inflammatory response during the early and late phases of infection. The bactericidal and inflammatory response of infected macrophages was progressively downregulated, while the number of THP-1 cells heavily loaded with live bacteria increased over time postinfection. Two of the main toxins of <i>B. pertussis</i>, pertussis toxin (Ptx) and adenylate cyclase (CyaA), were found to be involved in manipulating the host cell response. Therefore, failure to express either toxin proved detrimental to the development of intracellular infections by those bacteria. Taken together, these results support the relevance of host defense gene manipulation to the outcome of the interaction between <i>B. pertussis</i> and macrophages. Facultad de Ciencias Exactas Centro de Investigación y Desarrollo en Fermentaciones Industriales |
description |
<i>Bordetella pertussis</i>, the etiological agent of whooping cough, still causes outbreaks. We recently found evidence that <i>B. pertussis</i> can survive and even replicate inside human macrophages, indicating that this host cell might serve as a niche for persistence. In this work, we examined the interaction of <i>B. pertussis</i> with a human monocyte cell line (THP-1) that differentiates into macrophages in culture in order to investigate the host cell response to the infection and the mechanisms that promote that intracellular survival. To that end, we investigated the expression profile of a selected number of genes involved in cellular bactericidal activity and the inflammatory response during the early and late phases of infection. The bactericidal and inflammatory response of infected macrophages was progressively downregulated, while the number of THP-1 cells heavily loaded with live bacteria increased over time postinfection. Two of the main toxins of <i>B. pertussis</i>, pertussis toxin (Ptx) and adenylate cyclase (CyaA), were found to be involved in manipulating the host cell response. Therefore, failure to express either toxin proved detrimental to the development of intracellular infections by those bacteria. Taken together, these results support the relevance of host defense gene manipulation to the outcome of the interaction between <i>B. pertussis</i> and macrophages. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo 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://sedici.unlp.edu.ar/handle/10915/85803 |
url |
http://sedici.unlp.edu.ar/handle/10915/85803 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/issn/2049-632X info:eu-repo/semantics/altIdentifier/doi/10.1093/femspd/ftw073 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-sa/4.0/ Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) |
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openAccess |
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http://creativecommons.org/licenses/by-nc-sa/4.0/ Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) |
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