Tuberc Respir Dis.  1989 Mar;36(1):28-35. 10.4046/trd.1989.36.1.28.

Alpha-1-Antitrypsin in Human Bronchoalveolar Lavage: Effect of Smoking on Cell Populations and Elastase Inhibitory Capacity of Alpha-1-AT

Abstract

Many experimental animal study had confirmed the protease-antiprotease theory of emphysema that a destructive enzymatic activity against elastin is present within the lung in excess of antiprotease, especially alpha-1-AT, resulting in elastin fiber degradation and emphysema. Although cigarette smoking could lead to this imbalance, studies examining the presence of elastase in human bronchoalveolar lavage fluid had produced variable results. To further characterize the balance between protease and antiprotease in human BAL f1uid, we studied 42 subjects, both 20 of smoker and 22 of non smoker. The results were as follows. 1) Total amount of alpha.1-AT recovered from BAL fluid in smoker was 231.12 ± 53.85 μg compared with 221.50 ± 36.36 μg in non smoker (P > 0.05), corrected concentration of alpha-1-AT with volume in smoker was 5.18±1.10 μg/ml compared with 5.07 ± 0.7 μg/ml in non smoker (P> 0.05) and corrected concentration of alpha-1-AT with albumin in smoker was 136.00 ± 25.72 μg/ mg compared with 141.10 ± 31.6 μg/mg in non-smoker (P > 0.05) and the ratio of serum to BAL f1uid of albumin to alpha-1-AT in smoker was 2.79 ± 0.86 compared with 1.53 ± 0.27 in non-smoker (P > 0.05). 2) Total amount of elastase ingibitory capacity of alpha.1-AT in smoker was 1984.0 ± 587.2u compared with 7, 859.2 ± 2,089. 6u in non-smoker (P<0.01), corrected concentration of EIC in smoker was 480.0±113.6u/ml compared with 1,210 ± 166.4u/ml in non-smoker (P<0.01), corrected concentration with albumin in smoker was 60.98 ± 19.32u/ mg compared with 209.90 ± 49.38u/mg in non-smoker (P < 0.025) and the ratio of EIC to alpha-1-AT in smoker was 107.0 ± 25.6u/ mg compared with 264.0 ± 28.20u/mg in non-smoker (P < 0.025) In conclusion, Smoking cause the functional activity of alpha-l -AT to diminish in lavage f1uid.

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