Abstract
Elastase and antielastase activities were measured in bronchoalveolar lavage fluid (BALF) and their relationship to bronchoalveolar lavage (BAL) neutrophil numbers was assessed in order to determine whether the elevated BAL neutrophil count can predict a shift in the elastase/antielastase balance. BAL samples were obtained from 133 randomly selected patients undergoing diagnostic bronchoscopy with BAL. Elastase and antielastase activities were determined using the synthetic substrate MeO-Suc-Ala-Ala-Pro-Val-pNA. In a random subset of 24 samples, the antioxidant capacity was measured as the inhibition of peroxyl radical-mediated oxidation of B-phycoerythrin. Only 7 of the BAL samples exhibited measurable elastase activity and all but one of these had a BAL neutrophil count greater than 100 × 103/ml. Antielastase activity was measurable in 124 samples exhibiting no free elastase activity. There was a tendency for lower antielastase activity to be associated with higher neutrophil numbers, but this did not translate into a statistically significant correlation over all samples. There was no significant correlation between antioxidant capacity and either the neutrophil number or antielastase activity. It is concluded that BAL neutrophil numbers do not, in general, predict the status of elastase/antielastase balance in the epithelial lining fluid and that the antioxidant mechanisms in the epithelial lining fluid do not appear to be related to the antielastase capacity.
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References
Blake DR, Allen RE, Lunec J (1987) Free radicals in biological systems—a review oriented to inflammatory processes. Br Med Bull 43:371–385
Braun J, Dalhoff K, Lipp R, Eckmann C, Marre R, Wood WG, Wießmann K (1992) Myeloperoxidase, Lactoferrin und Elastase in Bronchoalveolärer Lavage und Plasma bei Pneumonie. Pneumologie 46;141–147
Carp H, Janoff A (1979) In vitro suppression of serum elastase inhibitory capacity by reactive oxygen species generated by phagocytosing polymorphonuclear leukocytes. J Clin Invest 63: 793–797
Christen S, Peterhans E, Stocker R (1990) Antioxidant activities of some tryptophan metabolites: possible implication for inflammatory diseases. Proc Natl Acad Sci USA 87:2506–2510
Eriksson S (1991) The potential role of elastase inhibitors in emphysema treatment. Eur Respir J 4:1041–1043
Fera T, Abboud RT, Richter A, Johal S (1986) Acute effect of smoking on elastase-like esterase activity and immunologic neutrophil elastase levels in bronchoalveolar lavage fluid. Am Rev Respir Dis 133:568–573
Fujita J, Nelson NL, Daughton DM, Dobry CA, Spurzem JR, Irino S, Rennard SI (1990) Evaluation of elastase and antielastase balance in patients with chronic bronchitis and pulmonary emphysema. Am Rev Respir Dis 142:57–62
Janoff A (1985) Elastases and emphysema. Am Rev Respir Dis 132:417–433
Janoff A, White R, Carp H, Harel S, Dearing R, Lee D (1979) Lung injury induced by leukocytic proteases. Am J Pathol 97:111–136
Morihara K, Tsuzuki H, Oka T, Inoue H, Ebata M (1965) Pseudomonas aeruginosa elastase, isolation, crystallization and preliminary characterization. J Biol Chem 240:3295–3304
Nathan CF, Tsunawaki S (1986) Secretion of toxic oxygen products by macrophages: regulatory cytokines and their effects on the oxidase. In: Evered D, Nugent J, O'Connor M (eds) Biochemistry of macrophages (Ciba Foundation Symposium 118). Pitman, London, pp 211–230
Neave HR (1981) Elementary statistics tables. Allen & Unwin, London
Pemberton PA, Stein PE, Pepys MB, Potter JM, Carrell RW (1988) Hormone binding globulins undergo serpin conformational change in inflammation. Nature 336:257–258
Renkema TE, Postma DS, Noordhoek JA, Sluiter HJ, Kauffman HF (1991) In vitro release of neutrophil elastase, myeloperoxidase and R-glucuronidase in patients with emphysema and healthy subjects. Eur Respir J 4:1237–1244
Schriver EE, Davidson JM, Sutcliffe MC, Swindell BB, Bernard GR (1992) Comparison of elastin peptide concentrations in body fluids from healthy volunteers, smokers, and patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 145:762–766
Senior RM, Connolly NL, Cury JD, Welgus HG, Campbell EJ (1989) Elastin degradation by human alveolar macrophages: a prominent role of metalloproteinase activity. Am Rev Respir Dis 139:1251–1256
Stockley RA, Burnett D (1993) Bronchoalveolar lavage and the study of proteinases and antiproteinases in the pathogenesis of chronic obstructive lung disease. Monaldi Arch Chest Dis 48:245–253
Stockley RA, Morrison HM (1990) Elastase inhibitors of the respiratory tract. Eur Respir J 9:9s–15s
Suter S, Schaad UB, Roux L, Nydetter UE, Waldvogel FA (1984) Granulocyte neutral proteases and Pseudomonas aeruginosa elastase as possible causes of airway damage in patients with cystic fibrosis. J Infect Dis 149:523–531
Wallaert B, Gressier B, Aerts C, Mizon C, Voisin C, Mizon J (1991) Oxidative inactivation of α1-proteinase inhibitor by alveolar macrophages from healthy smokers requires the presence of myeloperoxidase. Am J Respir Cell Mol Biol 5:437–444
Weiss SJ (1989) Tissue destruction by neutrophils. N Engl J Med 320:365–376
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Dent, G., Rabe, K.F. & Magnussen, H. Relationship between bronchoalveolar lavage neutrophil numbers and lavage fluid elastase and antielastase activities. Lung 173, 165–175 (1995). https://doi.org/10.1007/BF00175657
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DOI: https://doi.org/10.1007/BF00175657