Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation.

SANTUCCI NATALIA; DIAZ ARIANA; BIANCHI ERNESTO; SPINELLI SILVANA; D'ATTILIO LUCIANO; BONGIOVANNI BETTINA; DÍDOLI GRISELDA; BRANDAN NADIA; NANNINI LUIS; BAY MARÍA LUISA; BOTTASSO OSCAR

INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE

INT UNION AGAINST TUBERCULOSIS LUNG DISEASE (I U A T L D)

Lugar: París; Año: 2014 vol. 18 p. 981 - 987

1027-3719

BACKGROUND: Tuberculosis (TB) is a infectious disease characterised by a profound immune-endocrine metabolic imbalance, including a diminution in leptin plasma levels. Leptin appears to be the link between nutritional status and the development of a protective immune response. O B J E C T IVE : To examine the effects of leptin on the proliferation and production of interferon-gamma (IFN-c) by peripheral blood mononuclear cells (PBMC) n TB patients and healthy controls stimulated with mycobacterial antigens with or without leptin. As macrophages are key cells in mycobacterial containment, the effect of leptin on the production of interleukin (IL) 1b and IL-1Ra by the monocytic cell line THP-1 was also studied. RESULT S : Leptin diminished the proliferative capacity of PBMC on mycobacterial stimulation, and had no effect on IFN-c production in terms of measurements in culture supernatants or intracytoplasmic analysis using flow cytometry. Real-time polymerase chain reaction studies of PBMC from TB patients revealed a preserved expression of leptin receptor. Furthermore, IL-1b and IL-1Ra secretion by THP-1 cells was not modified by leptin treatment. CONCLUSION: The study results do not support the utility of treatment with leptin to correct immune imbalances due to TB.