IFN-γ induces LL-37 but does not control the intracellular growth of M. tuberculosis in alveolar macrophages
Herrera, María Teresa , González, Yolanda , Juárez, Esmeralda
2018, Number 4
2018; 77 (4)
ABSTRACT
Interferon-γ (IFN-γ) is one of the most important cytokines in pulmonary tuberculosis immune responses. Its main function is to activate antimicrobial mechanisms in macrophages. Patients with IFN-γ deficiencies are unable to control M. tuberculosis, thus the addition of rhIFN-γ is an alternative treatment. 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.
KEYWORDS
Human alveolar macrophages, M. tuberculosis, rhIFN-γ, TNF-α, LL-37, IRGM.
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