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BioMed Research International
Volume 2014, Article ID 916521, 10 pages
Research Article

Differential Macrophage Response to Slow- and Fast-Growing Pathogenic Mycobacteria

1Departamento de Microbiologia, Escuela Nacional de Ciencias Biologicas (ENCB), Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico
2Departamento de Inmunobioquímica, Torre de Investigación, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes (INPer), Montes Urales 800, Colonia Lomas de Virreyes, 11000 México City, DF, Mexico
3Departamento de Inmunologia, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional (IPN), 11340 México City, DF, Mexico
4Departamento of Biomedicina Molecular, Centro de Investigacion y de Estudios Avanzados (CINVESTAV), IPN, 07360 México City, DF, Mexico

Received 5 February 2014; Revised 10 April 2014; Accepted 30 April 2014; Published 18 May 2014

Academic Editor: Angel Cataldi

Copyright © 2014 A. Cecilia Helguera-Repetto et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nontuberculous mycobacteria (NTM) have recently been recognized as important species that cause disease even in immunocompetent individuals. The mechanisms that these species use to infect and persist inside macrophages are not well characterised. To gain insight concerning this process we used THP-1 macrophages infected with M. abscessus, M. fortuitum, M. celatum, and M. tuberculosis. Our results showed that slow-growing mycobacteria gained entrance into these cells with more efficiency than fast-growing mycobacteria. We have also demonstrated that viable slow-growing M. celatum persisted inside macrophages without causing cell damage and without inducing reactive oxygen species (ROS), as M. tuberculosis caused. In contrast, fast-growing mycobacteria destroyed the cells and induced high levels of ROS. Additionally, the macrophage cytokine pattern induced by M. celatum was different from the one induced by either M. tuberculosis or fast-growing mycobacteria. Our results also suggest that, in some cases, the intracellular survival of mycobacteria and the immune response that they induce in macrophages could be related to their growth rate. In addition, the modulation of macrophage cytokine production, caused by M. celatum, might be a novel immune-evasion strategy used to survive inside macrophages that is different from the one reported for M. tuberculosis.