title: Adverse neuro-immune-endocrine interactions in patients with active tuberculosis.
abstract: The nervous, endocrine and immune systems play a crucial role in maintaining homeostasis and interact with each other for a successful defensive strategy against injurious agents. However, the situation is different in long-term diseases with marked inflammation, in which defensive mechanisms become altered. In the case of tuberculosis (TB), this is highlighted by several facts: an imbalance of plasma immune and endocrine mediators, that results in an adverse environment for mounting an adequate response against mycobacteria and controlling inflammation; the demonstration that dehidroepiandrosterone (DHEA) secretion by a human adrenal cell line can be inhibited by culture supernatants from Mycobacterium tuberculosis-stimulated peripheral blood mononuclear cells - PBMC - of TB patients, with this effect being partly reverted when neutralizing transforming growth factor-β in such supernantants; the in vitro effects of adrenal steroids on the specific immune response of PBMC from TB patients, that is a cortisol inhibition of mycobacterial antigen-driven lymphoproliferation and interferon-γ production as well as a suppression of TGF-β production in DHEA-treated PBMC; and lastly the demonstration that immune and endocrine compounds participating in the regulation of energy sources and immune activity correlated with the consumption state of TB patients. Collectively, immune-endocrine disturbances of TB patients are involved in critical components of disease pathology with implications in the impaired clinical status and unfavorable disease outcome. This article is part of a Special Issue entitled 'Neuroinflammation in neurodegeneration and neurodysfunction'.
authors.affiliation: Instituto de Inmunología, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Argentina. bottasso@uolsinectis.com.ar
authors.forename: Oscar
authors.initials: O
authors.lastname: Bottasso
authors.forename: María Luisa
authors.initials: ML
authors.lastname: Bay
authors.forename: Hugo
authors.initials: H
authors.lastname: Besedovsky
authors.forename: Adriana
authors.initials: A
authors.lastname: Del Rey
mesh_terms: D016207:Cytokines / Q000276:immunology; D003687:Dehydroepiandrosterone / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D015213:Neuroimmunomodulation; D013315:Stress, Psychological / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology; D014397:Tuberculosis, Pulmonary / Q000276:immunology*
chemical_list: D016207:Cytokines; D016212:Transforming Growth Factor beta; D003687:Dehydroepiandrosterone