RESEARCH ARTICLE


The Toll-like Receptor 2/6 Ligand MALP-2 Reduces the Viability of Mycobacterium tuberculosis in Murine Macrophages



Carla Palma1, *, Elisabetta Iona1, Thomas Ebensen2, Carlos A Guzman2, Antonio Cassone1
1 Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, Rome, Italy
2 Department of Vaccinology an Applied Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany


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© Palma et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, Viale Regina Elena, 299 - 00161 Rome, Italy; E-mail: carla.palma@iss.it


Abstract

Toll-like receptors (TLRs) sense conserved structures of pathogens and influence macrophage functions. Here we investigated the impact of TLR signaling on the modulation of macrophage defense mechanisms against infection of Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis. We found that a synthetic derivative of the TLR2/6 agonist MALP-2 and the potent TLR4 agonist lipopolysaccharide inhibited the intracellular growth of MTB in murine macrophages. Likely the microbicidal effect was mediated by production of nitric oxide while it is still unclear the role played by release of TNF-α , IL-6, MIP-1β and IL-10. These results suggest that the activation of microbicidal defense via TLR ligands is an appealing target for the establishment on immune intervention against tuberculosis.

Key Words: Mycobacterium tuberculosis, Toll-like receptor ligands, nitric oxide, cytokines, macrophages, killing mechanisms.