Related Experiment Video
Updated: Feb 14, 2026
Local Anesthetic Thoracoscopy for Undiagnosed Pleural Effusion
Published on: November 10, 2023
The neuro-endocrine-immune relationship in pulmonary and pleural tuberculosis: a better local profile in pleural
L D'Attilio1, A Díaz1, R D V Fernández1
1lnstituto de Inmunología Clínica y Experimental de Rosario, Universidad Nacional de Rosario, Consejo Nacional de Investigaciones Científicas y Técnicas, Rosario.
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.
Related Concept Videos
01:25Pleural Effusion I: Introduction
There are two main types of pleural effusion: transudative and exudative. They are differentiated using Light's...
01:30Pleural Disorders: Types and Brief Description
01:28Pleural Effusion II: Symptoms and Management
A pleural effusion is the abnormal collection of fluid between the parietal and visceral pleura layers of tissue that form the lining of the lungs and chest cavity. It can occur independently or due to surrounding parenchymal diseases, such as infection, malignancy, or inflammatory conditions.
Clinical Manifestations:
01:29Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
01:28Pulmonary Tuberculosis II
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
01:28Pulmonary Tuberculosis V
Latent tuberculosis infection occurs when TB bacteria are present in a person's body, but are not causing illness or symptoms. It is not contagious, and preventive treatment is crucial to avoid the...