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Palma C, Iona E, Ebensen T, et al. The toll-like receptor 2/6 ligand MALP-2 reduces the viability of Mycobacterium tuberculosis in murine macrophages. Open Microbiol J. 2009;3:47-52doi: 10.2174/1874285800903010047.
Palma, C., Iona, E., Ebensen, T., Guzman, C. A., & Cassone, A. (2009). The toll-like receptor 2/6 ligand MALP-2 reduces the viability of Mycobacterium tuberculosis in murine macrophages. The open microbiology journal, 347-52. https://doi.org/10.2174/1874285800903010047
Palma, Carla, et al. "The toll-like receptor 2/6 ligand MALP-2 reduces the viability of Mycobacterium tuberculosis in murine macrophages." The open microbiology journal vol. 3 (2009): 47-52. doi: https://doi.org/10.2174/1874285800903010047
Palma C, Iona E, Ebensen T, Guzman CA, Cassone A. The toll-like receptor 2/6 ligand MALP-2 reduces the viability of Mycobacterium tuberculosis in murine macrophages. Open Microbiol J. 2009 Apr 03;3:47-52. doi: 10.2174/1874285800903010047. PMID: 19471610; PMCID: PMC2685717.
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Open Microbiol J. 2009 Apr 03;3:47-52. doi: 10.2174/1874285800903010047.

The toll-like receptor 2/6 ligand MALP-2 reduces the viability of Mycobacterium tuberculosis in murine macrophages.

The open microbiology journal

Carla Palma, Elisabetta Iona, Thomas Ebensen, Carlos A Guzman, Antonio Cassone

Affiliations

  1. Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, Rome, Italy. [email protected]

PMID: 19471610 PMCID: PMC2685717 DOI: 10.2174/1874285800903010047

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.

Keywords: Mycobacterium tuberculosis; Toll-like receptor ligands; cytokines; killing mechanisms.; macrophages; nitric oxide

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