An analysis of the immune-endocrine changes occurring in tuberculosis patients from the time of disease diagnosis to treatment completion and clinical recovery

DIAZ A; D´ATTILIO L; BONGIOVANNI B; SANTUCCI N; DIDOLI G; LIOI S; MASSONI C; DANIELLE S; RADCLIFFE S; GARDEÑEZ W; BRANDAM N; NANNINI L; BOGUE C; MARCHESINI M; BOTTASSO O; BAY ML

Medellín

Congreso; 11th Congress of the Latin American Association of Immunology (ALAI); 2015

Sociedad Latinoamericana de Inmunología

Tuberculosis (TB) mainly caused by Mycobacterium tuberculosis (Mtb) is a major health problem not only for its worldwide distribution but also for its morbidity and at times fatal course. While the cellular immune response (IR) is critical for containment and resolution of this infectious process, immune-mediated reactions can also lead to tissue pathology. We have earlier demonstrated that patients with pulmonary TB, at the time of diagnosis, showed a significant neuro-immune-endocrine imbalance. Briefly, patients had increased plasma levels of cortisol, pro- and anti-inflammatory cytokines together with impaired cellular IR and markedly decreased dehydroepiandrosterone (DHEA) amounts, resulting in an unbalanced cortisol/DHEA ratio. In terms of immune influences, cortisol inhibits the production of pro-inflammatory cytokines and the development of the cellular IR, whereas DHEA displays anti-inflammatory effects and promotes Th1 response. Extending these observations and given the relevance of the broad defensive response in infectious pathology we now investigated the immune-endocrine profile of TB patients from the time of disease diagnosis to treatment completion and clinical recovery. We sought to find out whether any of the immune-endocrine parameters under analysis (hormones, cytokines, acute phase proteins, lymphocyte populations -regulatory T cells-) could emerge as a biomarker of the disease course. Blood samples from 26 healthy controls (HCo) and 24 TB patients, HIV negative showing no sex or age differences were studied. Patients were bled at the time of diagnosis (T0) and 2 (T2), 4 (T4) and 6 months (T6) after the initiation of specific treatment, as well as 3 months following its completion (T9). At T0 patients showed increased plasma levels of interleukin 6 (IL-6, vs. HCo p