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 |
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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. |
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ISSN: | 0012-3692 1931-3543 |
DOI: | 10.1378/chest.117.1.103 |