Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape
- Autores
- Romero, María Mercedes; Balboa, Luciana; Basile, Juan Ignacio; López, Beatriz; Ritacco, Viviana; de la Barrera, Silvia; Sasiain, María C.; Barrera, Lucía; Alemán, Mercedes
- Año de publicación
- 2012
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Fil: Romero, María Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Fil: Balboa, Luciana. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Fil: Basile, Juan Ignacio. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Fil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
Fil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
Fil: de la Barrera, Silvia. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Fil: Sasiain, María C. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Fil: Barrera, Lucía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
Fil: Alemán, Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
Tuberculosis pathogenesis was earlier thought to be mainly related to the host but now it appears to be clear that bacterial factors are also involved. Genetic variability of Mycobacterium tuberculosis (Mtb) could be slight but it may lead to sharp phenotypic differences. We have previously reported that nonopsonized Mtb H37Rv induce apoptosis of polymorphonuclear neutrophils (PMNs) by a mechanism that involves the p38 pathway. Here we evaluated the capability to induce PMN apoptosis of two prevalent Mtb lineages in Argentina, the Latin America and Mediterranean (LAM), and Haarlem, using the H37Rv as a reference strain. Results showed that LAM strains strongly induced apoptosis of PMN which correlated with the induction of reactive oxygen species (ROS) production and p38 activation. Interestingly, the highly prosperous multidrug-resistant M strain, belonging to the Haarlem lineage, lacked the ability to activate and to induce PMN apoptosis as a consequence of (1) a weak ROS production and (2) the contribution of antiapoptotic mechanisms mediated at least by ERK. Although with less skill, M is able to enter the PMN so that phenotypic differences could lead PMN to be a reservoir allowing some pathogens to prevail and persist over other strains in the community. - Materia
-
Mycobacterium tuberculosis
Neutrófilos
Estallido Respiratorio
Apoptosis - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- Repositorio
- Institución
- Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"
- OAI Identificador
- oai:sgc.anlis.gob.ar:123456789/2288
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Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escapeRomero, María MercedesBalboa, LucianaBasile, Juan IgnacioLópez, BeatrizRitacco, Vivianade la Barrera, SilviaSasiain, María C.Barrera, LucíaAlemán, MercedesMycobacterium tuberculosisNeutrófilosEstallido RespiratorioApoptosisFil: Romero, María Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Fil: Balboa, Luciana. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Fil: Basile, Juan Ignacio. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Fil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.Fil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.Fil: de la Barrera, Silvia. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Fil: Sasiain, María C. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Fil: Barrera, Lucía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.Fil: Alemán, Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.Tuberculosis pathogenesis was earlier thought to be mainly related to the host but now it appears to be clear that bacterial factors are also involved. Genetic variability of Mycobacterium tuberculosis (Mtb) could be slight but it may lead to sharp phenotypic differences. We have previously reported that nonopsonized Mtb H37Rv induce apoptosis of polymorphonuclear neutrophils (PMNs) by a mechanism that involves the p38 pathway. Here we evaluated the capability to induce PMN apoptosis of two prevalent Mtb lineages in Argentina, the Latin America and Mediterranean (LAM), and Haarlem, using the H37Rv as a reference strain. Results showed that LAM strains strongly induced apoptosis of PMN which correlated with the induction of reactive oxygen species (ROS) production and p38 activation. Interestingly, the highly prosperous multidrug-resistant M strain, belonging to the Haarlem lineage, lacked the ability to activate and to induce PMN apoptosis as a consequence of (1) a weak ROS production and (2) the contribution of antiapoptotic mechanisms mediated at least by ERK. Although with less skill, M is able to enter the PMN so that phenotypic differences could lead PMN to be a reservoir allowing some pathogens to prevail and persist over other strains in the community.2012info:ar-repo/semantics/articuloinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://downloads.hindawi.com/journals/jir/2012/152546http://sgc.anlis.gob.ar/handle/123456789/228810.1155/2012/152546Clinical & developmental immunologyenginfo:eu-repo/semantics/openAccessreponame:Sistema de Gestión del Conocimiento ANLIS MALBRÁNinstname:Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"instacron:ANLIS2025-09-29T14:30:45Zoai:sgc.anlis.gob.ar:123456789/2288Institucionalhttp://sgc.anlis.gob.ar/Organismo científico-tecnológicoNo correspondehttp://sgc.anlis.gob.ar/oai/biblioteca@anlis.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:a2025-09-29 14:30:45.496Sistema de Gestión del Conocimiento ANLIS MALBRÁN - Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"false |
dc.title.none.fl_str_mv |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
title |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
spellingShingle |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape Romero, María Mercedes Mycobacterium tuberculosis Neutrófilos Estallido Respiratorio Apoptosis |
title_short |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
title_full |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
title_fullStr |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
title_full_unstemmed |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
title_sort |
Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape |
dc.creator.none.fl_str_mv |
Romero, María Mercedes Balboa, Luciana Basile, Juan Ignacio López, Beatriz Ritacco, Viviana de la Barrera, Silvia Sasiain, María C. Barrera, Lucía Alemán, Mercedes |
author |
Romero, María Mercedes |
author_facet |
Romero, María Mercedes Balboa, Luciana Basile, Juan Ignacio López, Beatriz Ritacco, Viviana de la Barrera, Silvia Sasiain, María C. Barrera, Lucía Alemán, Mercedes |
author_role |
author |
author2 |
Balboa, Luciana Basile, Juan Ignacio López, Beatriz Ritacco, Viviana de la Barrera, Silvia Sasiain, María C. Barrera, Lucía Alemán, Mercedes |
author2_role |
author author author author author author author author |
dc.subject.none.fl_str_mv |
Mycobacterium tuberculosis Neutrófilos Estallido Respiratorio Apoptosis |
topic |
Mycobacterium tuberculosis Neutrófilos Estallido Respiratorio Apoptosis |
dc.description.none.fl_txt_mv |
Fil: Romero, María Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Fil: Balboa, Luciana. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Fil: Basile, Juan Ignacio. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Fil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina. Fil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina. Fil: de la Barrera, Silvia. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Fil: Sasiain, María C. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Fil: Barrera, Lucía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina. Fil: Alemán, Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. Tuberculosis pathogenesis was earlier thought to be mainly related to the host but now it appears to be clear that bacterial factors are also involved. Genetic variability of Mycobacterium tuberculosis (Mtb) could be slight but it may lead to sharp phenotypic differences. We have previously reported that nonopsonized Mtb H37Rv induce apoptosis of polymorphonuclear neutrophils (PMNs) by a mechanism that involves the p38 pathway. Here we evaluated the capability to induce PMN apoptosis of two prevalent Mtb lineages in Argentina, the Latin America and Mediterranean (LAM), and Haarlem, using the H37Rv as a reference strain. Results showed that LAM strains strongly induced apoptosis of PMN which correlated with the induction of reactive oxygen species (ROS) production and p38 activation. Interestingly, the highly prosperous multidrug-resistant M strain, belonging to the Haarlem lineage, lacked the ability to activate and to induce PMN apoptosis as a consequence of (1) a weak ROS production and (2) the contribution of antiapoptotic mechanisms mediated at least by ERK. Although with less skill, M is able to enter the PMN so that phenotypic differences could lead PMN to be a reservoir allowing some pathogens to prevail and persist over other strains in the community. |
description |
Fil: Romero, María Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina. |
publishDate |
2012 |
dc.date.none.fl_str_mv |
2012 |
dc.type.none.fl_str_mv |
info:ar-repo/semantics/articulo info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
https://downloads.hindawi.com/journals/jir/2012/152546 http://sgc.anlis.gob.ar/handle/123456789/2288 10.1155/2012/152546 |
url |
https://downloads.hindawi.com/journals/jir/2012/152546 http://sgc.anlis.gob.ar/handle/123456789/2288 |
identifier_str_mv |
10.1155/2012/152546 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Clinical & developmental immunology |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.source.none.fl_str_mv |
reponame:Sistema de Gestión del Conocimiento ANLIS MALBRÁN instname:Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" instacron:ANLIS |
reponame_str |
Sistema de Gestión del Conocimiento ANLIS MALBRÁN |
collection |
Sistema de Gestión del Conocimiento ANLIS MALBRÁN |
instname_str |
Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" |
instacron_str |
ANLIS |
institution |
ANLIS |
repository.name.fl_str_mv |
Sistema de Gestión del Conocimiento ANLIS MALBRÁN - Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán" |
repository.mail.fl_str_mv |
biblioteca@anlis.gov.ar |
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1844621860072849408 |
score |
12.559606 |