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Clinical Investigations: TUBERCULOSIS |

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*

Thomas C. Y. Tsao, MD, FCCP; Ji-hong Hong, MD, PhD; Li-Fu Li, MD; Meng-Jer Hsieh, MD; Shuen-Kuei Liao, PhD; Kenneth S. S. Chang, MD, PhD
Author and Funding Information

*From the Division of Pulmonary and Critical Care Medicine (Drs. Tsao, Hong, Li, and Hsieh), Chang Gung Memorial Hospital, Taipei, and the Graduate Institute of Clinical Medicine (Drs. Liao and Chang), Chang Gung University, Linko, Taiwan.

Correspondence to: Thomas C.Y. Tsao, MD, Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, 199 Tun-Hwa North Rd, Taipei, Taiwan; e-mail: drtsao@adm.cgmh.com.tw



Chest. 2000;117(1):103-109. doi:10.1378/chest.117.1.103
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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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