Endocrine and cytokine responses in humans with pulmonary tuberculosis

DEL REY A; MAHUAD C; BOZZA V; BOGUE C; FARRONI M; BAY ML; BOTTASSO O; BESEDOVSKY H

BRAIN BEHAVIOR AND IMMUNITY

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2007 vol. 21 p. 171 - 179

0889-1591

Endocrine responses during chronic infections such as lung tuberculosis are poorly characterized. Hormonal changes are likely to occur since some of the cytokines produced during this disease could aVect endocrine mechanisms that, in turn, inXuence the course of nfectious/inXammatory processes. A main purpose of this work was to study endocrine responses involving pituitary, adrenal, gonadal, and thyroid hormones in parallel to IFN-, IL-10, and IL-6 levels in tuberculosis patients with diVerent degree of pulmonary involvement. We have also studied whether products derived from peripheral immune cells obtained from the patients can aVect the in vitro production of adrenal steroids. The population studied comprised HIV-negative newly diagnosed, untreated male patients with mild, moderate, and advanced lung tuberculosis, and matched, healthy controls. IFN-, IL-10, and IL-6 levels were elevated in patients with tuberculosis. Dehydroepiandrosterone and testosterone levels were profoundly decreased and growth hormone levels were markedly elevated in patients, in parallel to modest increases in cortisol, estradiol, prolactin, and thyroid hormone concentrations. Supernatants of peripheral blood mononuclear cells obtained from the patients and stimulated in vitro with Mycobacterium tuberculosis antigens signiWcantly inhibited dehydroepiandrosterone secretion by the human adrenal cell line NCI-H295-R. These results support the hypothesis that at least some of the endocrine changes observed in the patients may be mediated by endogenous cytokines. The endocrine proWle of tuberculosis patients would favor a reduction of protective cell-mediated immunity and an exacerbation of inXammation leading to perpetuation of the lung injury and to the hypercatabolic condition that characterizes this disease.Vect endocrine mechanisms that, in turn, inXuence the course of nfectious/inXammatory processes. A main purpose of this work was to study endocrine responses involving pituitary, adrenal, gonadal, and thyroid hormones in parallel to IFN-, IL-10, and IL-6 levels in tuberculosis patients with diVerent degree of pulmonary involvement. We have also studied whether products derived from peripheral immune cells obtained from the patients can aVect the in vitro production of adrenal steroids. The population studied comprised HIV-negative newly diagnosed, untreated male patients with mild, moderate, and advanced lung tuberculosis, and matched, healthy controls. IFN-, IL-10, and IL-6 levels were elevated in patients with tuberculosis. Dehydroepiandrosterone and testosterone levels were profoundly decreased and growth hormone levels were markedly elevated in patients, in parallel to modest increases in cortisol, estradiol, prolactin, and thyroid hormone concentrations. Supernatants of peripheral blood mononuclear cells obtained from the patients and stimulated in vitro with Mycobacterium tuberculosis antigens signiWcantly inhibited dehydroepiandrosterone secretion by the human adrenal cell line NCI-H295-R. These results support the hypothesis that at least some of the endocrine changes observed in the patients may be mediated by endogenous cytokines. The endocrine proWle of tuberculosis patients would favor a reduction of protective cell-mediated immunity and an exacerbation of inXammation leading to perpetuation of the lung injury and to the hypercatabolic condition that characterizes this disease.