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Gamma-interferon and soluble interleukin 2 receptor in tuberculous pleural effusion
1Department of Internal Medicine, Kangnam St. Mary's Hospital, Catholic University School of Medicine, 505 Banpo-Dong, Seocho-Ku, Seoul 137-040, Korea.
Insights
In pulmonary tuberculosis, T cell responses are lower in the blood but higher in pleural fluid. Elevated levels of interferon-gamma and soluble interleukin-2 receptor in pleural effusion may predict residual pleural thickening after treatment.
Area of Science:
- Immunology
- Infectious Diseases
- Pulmonology
Background:
- T cell responses are crucial in tuberculosis (TB) pathogenesis.
- Distinguishing systemic from local immune responses in TB is essential for understanding disease progression and outcomes.
- Residual pleural thickening (RPT) is a common complication of tuberculous pleural effusion (TPE).
Purpose of the Study:
- To analyze the differences between systemic and local T cell responses in pulmonary tuberculosis.
- To investigate the association between pleural fluid immune markers and the development of RPT.
- To evaluate the utility of interferon-gamma (IFN-γ) and soluble interleukin-2 receptor (sIL-2R) as markers for RPT.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure IFN-γ and sIL-2R levels.
- Measurements were performed on peripheral blood mononuclear cell (PBMC) culture supernatants and pleural effusion (PE) samples.
- Study groups included patients with active pulmonary TB (with/without PE), non-TB pleural effusion, and healthy controls.
Main Results:
- IFN-γ and sIL-2R levels in PBMC supernatants were lower in TB patients compared to healthy controls.
- Conversely, IFN-γ and sIL-2R levels in PE were higher in TB patients than in non-TB pleural effusion.
- TB patients with PE had lower PBMC levels of IFN-γ and sIL-2R than those without PE.
- Higher IFN-γ and sIL-2R levels in PE correlated with lower levels in PBMC supernatants.
- Patients who developed RPT had significantly higher IFN-γ and sIL-2R levels in their PE.
Conclusions:
- Diminished systemic Th1 response in TB may result from the sequestration of activated T cells at the disease site.
- IFN-γ and sIL-2R levels in pleural effusion are potential biomarkers for predicting post-treatment residual pleural thickening.
Abstract:
To analysis the difference between systemic and local pleural T cell response in pulmonary tuberculosis, we analyzed interferon (IFN)-gamma and soluble interleukin-2 receptor (sIL-2R) in peripheral blood mononuclear cells (PBMC) culture supernatants and in pleural effusion (PE). We also investigated the association of pleural INF-gamma and sIL-2R levels with development of residual pleural thickening (RPT). The subjects in this study included patients with active pulmonary tuberculosis with or without PE (n = 46), those with nontuberculous PE (n = 32), and healthy tuberculin reactors (n = 20). Measurement of IFN-gamma and sIL-2R were made by ELISA. In pulmonary tuberculosis, IFN-gamma and sIL-2R concentrations in PBMC culture supernatants were lower than those of healthy tuberculin reactors (IFN-gamma; 258.4 +/-111.5 pg/mL versus 2792.5 +/-633.2 pg/mL, sIL-2R; 1465.0 +/-144.4 pg/mL versus 4777.1 +/-178.5 pg/mL, p < 0.05), whereas IFN-gamma and sIL-2R concentrations in PE were higher than those from nontuberculous pleural effusion (IFN-gamma; 1154.4 +/-252.4 pg/mL versus 292.0 +/-68.9 pg/mL, sIL-2R; 9805.2 +/-978.9 pg/mL versus 3426.7 +/-695.6 g/mL, p < 0.05). IFN-gamma and sIL-2R in PBMC culture supernatants were significantly lower in tuberculat patients with PE than those without PE, and the patients with a high value of IFN-gamma or sIL-2R in PE showed a low value of IFN-gamma or sIL-2R in PBMC culture supernatant, respectively. Patients with RPT had significantly higher IFN-gamma and sIL-2R values in their PE compared with those without RPT. These findings suggest that diminished systemic Th1 response in tuberculosis results from the accumulation of activated Th1 cell to the disease site, and that levels of IFN-gamma and sIL-2R in PE are useful posttreatment markers of RPT.
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