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.