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The Adrenal Steroid Response during Tuberculosis and Its Effects on the Mycobacterial-driven IFN-γ Production of Patients and Their Household Contacts


Address for correspondence: Oscar Bottasso, Institute of Immunology, School of Medical Sciences, National University of Rosario, Santa Fe 3100, Rosario, Argentina. Voice: +54 341 4804559; fax: +54 341 34804569.


Earlier studies revealed that patients with tuberculosis (TB) have imbalanced immunoendocrine responses and that adrenal steroids [cortisol and dehydroepiandrosterone (DHEA)] can modify their specific cell-mediated immune response. Because most household contacts (HHCs) of contagious TB patients develop a subclinical and self-controlled process (latent TB), we studied some features of their immune and endocrine responses, particularly those related to the hypothalamic–pituitary–adrenal axis. Nineteen HHCs, 24 untreated TB patients (15 moderate, 9 advanced), and 18 healthy controls of similar age were studied. Patients had increased and reduced levels of cortisol and DHEA, respectively. DHEA levels were also reduced in HHCs. Stimulation of peripheral blood mononuclear cells (PBMC) with Mycobacterium tuberculosis sonicate resulted in increased in vitro lymphoproliferation in HHCs, while advanced patients showed the lowest response. Significantly higher amounts of interferon (IFN)-γ were detected in supernatants from stimulated PBMC of HHCs when compared to controls and TB patients. Addition of cortisol to the cultures inhibited mycobacterial antigen-driven IFN-γ production in all groups, although HHC supernatant contained significantly higher concentrations. In contrast, addition of DHEA to cultures of cells from HHCs resulted in increased IFN-γ levels. These results suggest the existence of a particular immunoendocrine relation assuring a preserved IFN-γ production in healthy housemates of TB patients.