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

SANTUCCI N; DIAZ A; BIANCHI E; SPINELLI S; D´ATTILIO L; BONGIOVANNI B; DIDOLI G; BRANDAM N; NANNINI L; BAY ML; BOTTASSO O

INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE

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

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

1027-3719

BACKGROUND: Tuberculosis (TB) is a infectious diseasecharacterised by a profound immune-endocrinemetabolic imbalance, including a diminution in leptinplasma levels. Leptin appears to be the link betweennutritional status and the development of a protectiveimmune response.O B J E C T IVE : To examine the effects of leptin on theproliferation and production of interferon-gamma(IFN-c) by peripheral blood mononuclear cells (PBMC)in TB patients and healthy controls stimulated withmycobacterial antigens with or without leptin. Asmacrophages are key cells in mycobacterial containment,the effect of leptin on the production ofinterleukin (IL) 1b and IL-1ra by the monocytic cellline THP-1 was also studied.RESULT S : Leptin diminished the proliferative capacityof PBMC on mycobacterial stimulation, and had noeffect on IFN-c production in terms of measurements inculture supernatants or intracytoplasmic analysis usingflow cytometry. Real-time polymerase chain reactionstudies of PBMC from TB patients revealed a preservedexpression of leptin receptor. Furthermore, IL-1b and IL-1ra secretion by THP-1 cells was not modified by leptintreatment.CONCLUSION: The study results do not support theutility of treatment with leptin to correct immuneimbalances due to TB.