Abstract
Our earlier studies in tuberculosis (TB) patients indicate that in those where the process evolves to a larger pulmonary involvement, the immune endocrine response may promote an unfavorable environment. Chronic infectious diseases, and their persistent proinflammatory response, may affect mucosal barriers integrity favoring the translocation of gastrointestinal bacteria, leading to an increase of circulating lipopolysaccharides (LPS). Consequently, we quantified LPS levels in TB patients, with different degrees of pulmonary involvement, and controls (Co) and analyzed the possible relationship between LPS and inflammatory mediators i.e., C reactive protein (CRP), interleukin 6 (IL-6) and Interferon-gamma (IFN-γ), Erythrocyte Sedimentation Rate (ESR), steroid hormones (Cortisol and Dehydroepiandrosterone, DHEA), and inflammatory transcripts from peripheral blood mononuclear cells (IL-1β, IL-6, IFN-γ). LPS was assessed by the Limulus amoebocyte lysate assay and the ELISA technique was used to quantify hormones and cytokines in the plasma samples. Cytokine transcripts from PBMC were evaluated by qRT-PCR. Non-parametric tests were used. LPS levels were increased in TB patients, as did levels of CRP, IL-6, IFN-γ, cortisol and ESR. Severe patients had the highest amounts of circulating LPS; with moderate and severe cases showing much higher levels of CRP, ESR, IL-6, IFN-γ and cortisol/DHEA ratio, as an endocrine imbalance. Only in PBMC from severe cases was mRNA for IL-1β increased. Correlation analysis showed that levels of LPS from severe patients were positively associated with IL-6 and IFN-γ plasma concentrations and with IL-1β transcripts, while IL-6 had a positive correlation with the cortisol/DHEA ratio. The higher levels of circulating LPS during progressive TB may emerge as a contributing factor for the persistence of the greater immune endocrine imbalance distinctive of advanced disease, which might suggest a vicious cycle among LPS, inflammation and endocrine imbalance.
Highlights
The bidirectional communication between the neuroendocrine and immune systems is a fact that medicine has recognized for a long time as revealed by a diverse series of studies both in humans and in experimental models
Within the context of the immune endocrine interactions, we showed that TB patients had reduced levels of dehydroepiandrosterone (DHEA), in presence of higher concentrations of proinflammatory mediators and cortisol, even further in patients with progressive disease along with a more unbalanced Cortisol/DHEA ratio [3, 4]
In the present work we provide evidence demonstrating that plasma LPS levels were increased in TB patients, as did levels of inflammatory mediators (CRP, interleukin 6 (IL-6), IFN-γ) and the Erythrocyte Sedimentation Rate (ESR)
Summary
The bidirectional communication between the neuroendocrine and immune systems is a fact that medicine has recognized for a long time as revealed by a diverse series of studies both in humans and in experimental models. Many studies show that the products of the immune response modify the functioning of the neuroendocrine system, while a no lesser number of findings indicate, in turn, that hormones directly alter the activity of immune cells and the course of diseases with inflammatory, autoimmune, or infectious background. This cross relationship between the immune and neuroendocrine systems is partly due to the stimulatory action of inflammatory cytokines on the hypothalamus-pituitary-adrenal (HPA) axis. Our studies in the case of TB indicate that the immune-endocrine interrelationships are certainly relevant in pathophysiological terms [3, 4]
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