info:eu-repo/semantics/article
The neuro-endocrine-immune relationship in pulmonary and pleural tuberculosis: A better local profile in pleural fluid
Fecha
2018-03Registro en:
D'attilio, Luciano David; Díaz, Ariana; Fernández, Rocío del Valle; Bongiovanni, Bettina; Santucci, Natalia Estefanía; et al.; The neuro-endocrine-immune relationship in pulmonary and pleural tuberculosis: A better local profile in pleural fluid; International Union Against Tuberculosis and Lung Disease; International Journal of Tuberculosis and Lung Disease; 22; 3; 3-2018; 321-327
1027-3719
1027-3719
CONICET Digital
CONICET
Autor
D'attilio, Luciano David
Díaz, Ariana
Fernández, Rocío del Valle
Bongiovanni, Bettina
Santucci, Natalia Estefanía
Dídoli, Griselda
Lioi, Susana
Gardeñez, W.
Naninni, J. L.
Del Rey, A.
Besedovsky, H.
Bottasso, Oscar Adelmo
Bay, Maria Luisa
Resumen
BACKGROUND: Tuberculosis (TB) is a major health problem worldwide. In TB, the immune and central nervous systems modulate each other. The two main components of this network are the hypothalamic-pituitary-adrenal axis (HPA) and autonomic nervous system (ANS). OBJECTIVE: To elucidate neuro-endocrine-immune (NEI) interactions in pulmonary (PTB) or pleural (PLTB) TB, we analysed the relationship among compounds from these systems. METHODS: We quantified levels of catecholamines, hormones and cytokines in plasma from patients with PTB (n = 46) or PLTB (n = 12) and controls (n = 32), and in the pleural fluid from PLTB patients. Transcript expression for genes involved in glucocorticoid-related function (quantitative real-time polymerase chain reaction) was also analysed in mononuclear cells (MCs) from peripheral blood (PBMC) or pleural effusion (PEMC) compartments. RESULTS: Both patient groups had increased plasma levels of pro- and anti-inflammatory cytokines, cortisol, growth hormone (GH) and dopamine, whereas insulin-like growth factor 1 (IGF-1) and dehydroepiandrosterone levels were decreased. The pleural fluid contained increased levels of pro-inflammatory cytokines, GH and IGF-1 and reduced levels of steroid hormones compared with their plasma counterparts. PBMCs from PTB patients had increased expression of transcripts for 11β-hydroxysteroid dehydrogenase (11βHSD1) and a decreased glucocorticoid receptor (GR) ratio (GRα/GRβ). In PLTB cases, expression of 11βHSD1 and GRα transcripts was higher in PEMCs. CONCLUSION: PTB patients seem to display adverse NEI dysregulation. Changes in pleural fluid are compatible with a more effective NEI reaction.