Clinical Isolates of Mycobacterium tuberculosis Differ in Their Ability to Induce Respiratory Burst and Apoptosis in Neutrophils as a Possible Mechanism of Immune Escape

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...

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Main Authors: María M. Romero, Luciana Balboa, Juan I. Basile, Beatriz López, Viviana Ritacco, Silvia S. de la Barrera, María C. Sasiain, Lucía Barrera, Mercedes Alemán
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2012/152546
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author María M. Romero
Luciana Balboa
Juan I. Basile
Beatriz López
Viviana Ritacco
Silvia S. de la Barrera
María C. Sasiain
Lucía Barrera
Mercedes Alemán
author_facet María M. Romero
Luciana Balboa
Juan I. Basile
Beatriz López
Viviana Ritacco
Silvia S. de la Barrera
María C. Sasiain
Lucía Barrera
Mercedes Alemán
author_sort María M. Romero
collection DOAJ
description 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.
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spelling doaj-art-8058ae6001764af7a88491f384588bb82025-02-03T05:46:02ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/152546152546Clinical Isolates of Mycobacterium tuberculosis Differ in Their Ability to Induce Respiratory Burst and Apoptosis in Neutrophils as a Possible Mechanism of Immune EscapeMaría M. Romero0Luciana Balboa1Juan I. Basile2Beatriz López3Viviana Ritacco4Silvia S. de la Barrera5María C. Sasiain6Lucía Barrera7Mercedes Alemán8IMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaServicio de Micobacterias, Hospital Malbrán, Pacheco de Melo 3081, 1425 Buenos Aires, ArgentinaServicio de Micobacterias, Hospital Malbrán, Pacheco de Melo 3081, 1425 Buenos Aires, ArgentinaIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaServicio de Micobacterias, Hospital Malbrán, Pacheco de Melo 3081, 1425 Buenos Aires, ArgentinaIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, ArgentinaTuberculosis 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.http://dx.doi.org/10.1155/2012/152546
spellingShingle María M. Romero
Luciana Balboa
Juan I. Basile
Beatriz López
Viviana Ritacco
Silvia S. de la Barrera
María C. Sasiain
Lucía Barrera
Mercedes Alemán
Clinical Isolates of Mycobacterium tuberculosis Differ in Their Ability to Induce Respiratory Burst and Apoptosis in Neutrophils as a Possible Mechanism of Immune Escape
Clinical and Developmental Immunology
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
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_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_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
url http://dx.doi.org/10.1155/2012/152546
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