Imbalances between tumor necrosis factor-alpha and its soluble receptor forms, and interleukin-1 beta and interleukin-1 receptor antagonist in BAL fluid of cavitary pulmonary tuberculosis

Citation
Tcy. Tsao et al., Imbalances between tumor necrosis factor-alpha and its soluble receptor forms, and interleukin-1 beta and interleukin-1 receptor antagonist in BAL fluid of cavitary pulmonary tuberculosis, CHEST, 117(1), 2000, pp. 103-109
Citations number
34
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
117
Issue
1
Year of publication
2000
Pages
103 - 109
Database
ISI
SICI code
0012-3692(200001)117:1<103:IBTNFA>2.0.ZU;2-V
Abstract
Objectives: We investigated the possibility that the large pulmonary cavity in tuberculosis (TB) lesions might result from imbalances between tumor ne crosis factor-alpha (TNF-alpha) and soluble TNF-alpha receptor forms (sTNF- RI and sTNF-RII), and interleukin-beta (IL-1 beta) and IL-1 receptor antago nist (IL-1RA) in sites of local inflammation, Patients and methods: BAL was performed in 32 patients with active pulmonar y TB, and the recovered BAL fluid (BALF) was examined for concentrations of TNF-alpha and its soluble receptor forms, IL-1 beta, and IL-IRA. Patients were classified into two groups: group 1, patients with a large cavity (gre ater than or equal to 4 cm) on chest radiographs (n = 15); and group 2, pat ients with a small cavity (< 4 cm; n = 3) or no cavity (n = 14) on chest ra diographs. Results: The concentrations of TNF-alpha, IL-1 beta, and IL-IRA in BALF wer e significantly higher in group 1 patients than in group 2 patients before standardization. The difference was also statistically significant for TNF- alpha and LL-IP after standardization with urea, Furthermore, group 1 patie nts had significantly higher ratios of TNF-alpha to sTNF-RI and sTNF-RII an d IL-1 beta to IL-1RA compared with group 2 patients, Conclusions: These findings suggest that the relative abundance of TNF-alph a and IL-1 beta associated with imbalances of secretion of soluble TNF-alph a receptor forms and IL-1RA may have caused tissue necrosis leading to cavi ty formation in patients with active pulmonary TB.