Increased soluble Fas ligand concentration in tuberculous pleural effusion.

Abstract

Tuberculous (TB) pleurisy results from a delayed hypersensitivity reaction involving macrophages, T-cells, and many cytokines (including tumor necrosis factor, interferon-gamma, and interleukin 1 and 2). Infection by Mycobacterium tuberculosis induces apoptosis in gamma/delta T-cells and macrophages. Fas ligand (FasL) is a type II membrane protein that plays an important role in the regulation of apoptosis and has an intimate relation with these cells and cytokines. A soluble form of FasL (sFasL) exists in a variety of human body fluids, including serum, pleural effusion, cerebral spinal fluid, and ocular fluid. Therefore, we hypothesized that Fas activity is elevated in TB pleurisy. This study investigated the concentration of sFasL in TB pleural effusions and compared it with expression of sFasL in various other pleural effusions.
Using an enzyme-linked immunosorbent assay, we investigated the sFasL concentrations of 80 pleural effusions from patients with various diagnoses.
The median sFasL concentration in the TB pleural effusion group was 104.91 pg/mL (n = 32). This was significantly higher than values in the transudate group (median value, 20.02 pg/mL, n = 9, p < 0.001) and patients with malignant effusion associated with adenocarcinoma of the lung (median value, 23.29 pg/mL, n = 14, p < 0.001). Lymphoproliferative disease could not be distinguished from TB based on sFasL concentrations in pleural effusion.
The sFasL concentration in TB pleural effusions is significantly higher than that in adenocarcinomatous pleural effusions, which are the most common malignant pleural effusions. This difference may serve as a diagnostic tool to differentiate these two most commonly encountered unexplained pleural effusions. Determination of the cellular source and the actual role of the abundant sFasL in TB pleurisy will require further investigation.