Objective:

To evaluate the effects of recombinant human IFN-γ (rhIFN-γ) on human alveolar macrophages infected with M. tuberculosis.

Methods:

We infected alveolar macrophages from healthy volunteers with M. tuberculosis H37Rv and treated them with rhIFN-γ to evaluate the gene expression of antimicrobial peptide LL-37 and the IRGM protein (related to autophagy) by real time PCR (qPCR), tumoral necrosis factor-α (TNF-α) production by ELISA and intracellular growth control by colony forming units (CFU) of M. tuberculosis.

Results:

Uninfected macrophages over expressed IRGM after rhIFN-γ treatment, whereas infected macrophages over expressed LL-37. However, the addition of rhIFN-γ did not have a significant effect on production TNF-α production and intracellular growth control of M. tuberculosis.

Conclusion:

Although LL-37 expression was induced, it was not associated with the killing of M. tuberculosis, suggesting that there are IFN-γ-independent mechanisms involved in the pathogen elimination.