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
Sistema de Gestión del Conocimiento ANLIS MALBRÁN
Institución
Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"
OAI Identificador
oai:sgc.anlis.gob.ar:123456789/2288
Acceder
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network_acronym_str SGCANLIS
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network_name_str Sistema de Gestión del Conocimiento ANLIS MALBRÁN
spelling 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:ANLIS2025-10-23T11:23:47Zoai: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:a2025-10-23 11:23:47.964Sistema 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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score 12.471625

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