dc.creatorRomero, María Mercedes
dc.creatorBalboa, Luciana
dc.creatorBasile, Juan Ignacio
dc.creatorLópez, Beatriz
dc.creatorRitacco, Viviana
dc.creatorde la Barrera, Silvia
dc.creatorSasiain, María C.
dc.creatorBarrera, Lucía
dc.creatorAlemán, Mercedes
dc.date2021-02-01T20:19:25Z
dc.date2021-02-01T20:19:25Z
dc.date2012
dc.date.accessioned2023-08-29T20:09:18Z
dc.date.available2023-08-29T20:09:18Z
dc.identifierhttps://downloads.hindawi.com/journals/jir/2012/152546
dc.identifierhttp://sgc.anlis.gob.ar/handle/123456789/2288
dc.identifier10.1155/2012/152546
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8520612
dc.descriptionFil: Romero, María Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionFil: Balboa, Luciana. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionFil: Basile, Juan Ignacio. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionFil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
dc.descriptionFil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
dc.descriptionFil: de la Barrera, Silvia. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionFil: Sasiain, María C. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionFil: Barrera, Lucía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Microbacterias; Argentina.
dc.descriptionFil: Alemán, Mercedes. Academia Nacional de Medicina. Instituto de Medicina Experimental; Argentina.
dc.descriptionTuberculosis 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.
dc.formatPDF
dc.languageen
dc.relationClinical & developmental immunology
dc.rightsopen
dc.subjectMycobacterium tuberculosis
dc.subjectNeutrófilos
dc.subjectEstallido Respiratorio
dc.subjectApoptosis
dc.titleClinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape
dc.typeArtículo


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