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Neumología y cirugía de tórax
versión impresa ISSN 0028-3746
Resumen
HERRERA, María Teresa; GONZALEZ, Yolanda y JUAREZ, Esmeralda. IFN-γ induces LL-37 but does not control the intracellular growth of M. tuberculosis in alveolar macrophages. Neumol. cir. torax [online]. 2018, vol.77, n.4, pp.267-275. ISSN 0028-3746.
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.
Palabras llave : Human alveolar macrophages; M. tuberculosis; rhIFN-γ; TNF-α; LL-37; IRGM.
