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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Wiley
2012-01-01
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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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id | doaj-art-8058ae6001764af7a88491f384588bb8 |
institution | Kabale University |
issn | 1740-2522 1740-2530 |
language | English |
publishDate | 2012-01-01 |
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series | Clinical and Developmental Immunology |
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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