title: Imbalances between tumor necrosis factor-alpha and its soluble receptor forms, and interleukin-1beta and interleukin-1 receptor antagonist in BAL fluid of cavitary pulmonary tuberculosis.
abstract: OBJECTIVE
  We investigated the possibility that the large pulmonary cavity in tuberculosis (TB) lesions might result from imbalances between tumor necrosis factor-alpha (TNF-alpha) and soluble TNF-alpha receptor forms (sTNF-RI and sTNF-RII), and interleukin-beta (IL-1beta) and IL-1 receptor antagonist (IL-1RA) in sites of local inflammation.
  
  
  METHODS
  BAL was performed in 32 patients with active pulmonary TB, and the recovered BAL fluid (BALF) was examined for concentrations of TNF-alpha and its soluble receptor forms, IL-1beta, and IL-1RA. Patients were classified into two groups: group 1, patients with a large cavity (> or = 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-alpha, IL-1beta, 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-alpha and IL-1beta after standardization with urea. Furthermore, group 1 patients had significantly higher ratios of TNF-alpha to sTNF-RI and sTNF-RII and IL-1beta to IL-1RA compared with group 2 patients.
  
  
  CONCLUSIONS
  These findings suggest that the relative abundance of TNF-alpha and IL-1beta associated with imbalances of secretion of soluble TNF-alpha receptor forms and IL-1RA may have caused tissue necrosis leading to cavity formation in patients with active pulmonary TB.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan. drtsao@adm.cgmh.com.tw
authors.forename: T C
authors.initials: TC
authors.lastname: Tsao
authors.forename: J h
authors.initials: Jh
authors.lastname: Hong
authors.forename: L F
authors.initials: LF
authors.lastname: Li
authors.forename: M J
authors.initials: MJ
authors.lastname: Hsieh
authors.forename: S K
authors.initials: SK
authors.lastname: Liao
authors.forename: K S
authors.initials: KS
authors.lastname: Chang
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015415:Biomarkers; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000166:cytology; D002452:Cell Count; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D013902:Radiography, Thoracic; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins / Q000378:metabolism*; D014397:Tuberculosis, Pulmonary / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha