Imbalances Between Tumor Necrosis Factor-α and Its Soluble Receptor Forms, and Interleukin-1β and Interleukin-1 Receptor Antagonist in BAL Fluid of Cavitary Pulmonary Tuberculosis

Objectives: We investigated the possibility that the large pulmonary cavity in tuberculosis (TB) lesions might result from imbalances between tumor necrosis factor-α (TNF-α) and soluble TNF-α receptor forms (sTNF-RI and sTNF-RII), and interleukin-β (IL-1β) and IL-1 receptor antagonist (IL-1RA)...

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Veröffentlicht in:Chest 2000-01, Vol.117 (1), p.103
Hauptverfasser: Thomas C. Y. Tsao, Ji-hong Hong, Li-Fu Li, Meng-Jer Hsieh, Shuen-Kuei Liao, Kenneth S. S. Chang
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Sprache:eng
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Zusammenfassung:Objectives: We investigated the possibility that the large pulmonary cavity in tuberculosis (TB) lesions might result from imbalances between tumor necrosis factor-α (TNF-α) and soluble TNF-α receptor forms (sTNF-RI and sTNF-RII), and interleukin-β (IL-1β) and IL-1 receptor antagonist (IL-1RA) in sites of local inflammation. Patients and methods: BAL was performed in 32 patients with active pulmonary TB, and the recovered BAL fluid (BALF) was examined for concentrations of TNF-α and its soluble receptor forms, IL-1β, and IL-1RA. Patients were classified into two groups: group 1, patients with a large cavity (≥ 4 cm) on chest radiographs (n = 15); and group 2, patients with a small cavity (< 4 cm; n = 3) or no cavity (n = 14) on chest radiographs. Results: The concentrations of TNF-α, IL-1β, and IL-1RA in BALF were significantly higher in group 1 patients than in group 2 patients before standardization. The difference was also statistically significant for TNF-α and IL-1β after standardization with urea. Furthermore, group 1 patients had significantly higher ratios of TNF-α to sTNF-RI and sTNF-RII and IL-1β to IL-1RA compared with group 2 patients. Conclusions: These findings suggest that the relative abundance of TNF-α and IL-1β associated with imbalances of secretion of soluble TNF-α receptor forms and IL-1RA may have caused tissue necrosis leading to cavity formation in patients with active pulmonary TB.
ISSN:0012-3692
1931-3543
DOI:10.1378/chest.117.1.103