ALPHA-1-PROTEASE INHIBITOR IN BRONCHIAL-ASTHMA - PHENOTYPES AND BIOCHEMICAL CHARACTERISTICS

被引:47
作者
GAILLARD, MC
KILROESMITH, TA
NOGUEIRA, C
DUNN, D
JENKINS, T
FINE, B
KALLENBACH, J
机构
[1] UNIV WITWATERSRAND,DEPT PULM,JOHANNESBURG 2193,SOUTH AFRICA
[2] S AFRICAN INST MED RES,SCH PATHOL,DEPT HUMAN GENET,NATL CTR OCCUPAT HLTH,JOHANNESBURG 2000,SOUTH AFRICA
来源
AMERICAN REVIEW OF RESPIRATORY DISEASE | 1992年 / 145卷 / 06期
关键词
D O I
10.1164/ajrccm/145.6.1311
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
The prevalence of the different phenotypes of alpha-1-protease inhibitor (alpha-1PI) was investigated in a group of go asthmatic patients and compared with that of a control group of 240 individuals representing the general population. The M2M2 phenotype occurred more frequently in the asthmatic group (p = 0.015). Plasma samples of 51 of the asthmatic patients randomly selected from the different phenotype groups identified were studied for the absolute plasma values of alpha-1-PI and the inhibitory capacity of plasma for porcine pancreatic elastase, and compared with those from 21 nonasthmatic individuals of the M1M1 phenotype. Although the asthmatic patients had higher absolute alpha-1PI values (p = 0.04), the plasma elastase inhibitory capacity was markedly reduced compared with the nonasthmatic subjects (p = 0.01). The functional efficiency of alpha-1PI from asthmatic patients of the M1M1, M1M2, and M2M2 phenotypes was significantly decreased compared with that of the nonasthmatic M1M1 individuals. Functional deficiency of alpha-1PI may be important in the pathogenesis of the inflammatory process that characterizes bronchial asthma.
引用
收藏
页码:1311 / 1315
页数:5
相关论文
共 40 条
[1]  
[Anonymous], 1956, NONPARAMETRIC STAT B
[2]  
BARNES PJ, 1989, NEW ENGL J MED, V321, P1517
[3]  
BARTER CE, 1976, AM REV RESPIR DIS, V113, P305
[4]   HUMAN-LEUKOCYTE AND PORCINE PANCREATIC ELASTASE - X-RAY CRYSTAL-STRUCTURES, MECHANISM, SUBSTRATE-SPECIFICITY, AND MECHANISM-BASED INHIBITORS [J].
BODE, W ;
MEYER, E ;
POWERS, JC .
BIOCHEMISTRY, 1989, 28 (05) :1951-1963
[5]  
BRANTLY M, 1988, AM J MED, V84, P13
[6]  
BUIST AS, 1979, AM REV RESPIR DIS, V120, P759
[7]   THE ROLE OF PLATELET-ACTIVATING-FACTOR IN INFLAMMATION [J].
CAMUSSI, G ;
TETTA, C ;
BAGLIONI, C .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1990, 57 (03) :331-338
[8]   TUMOR NECROSIS FACTOR STIMULATES HUMAN-NEUTROPHILS TO RELEASE LEUKOTRIENE-B4 AND PLATELET-ACTIVATING FACTOR - INDUCTION OF PHOSPHOLIPASE-A2 AND ACETYL-COA - 1-ALKYL-SN-GLYCERO-3-PHOSPHOCHOLINE O2-ACETYLTRANSFERASE ACTIVITY AND INHIBITION BY ANTIPROTEINASE [J].
CAMUSSI, G ;
TETTA, C ;
BUSSOLINO, F ;
BAGLIONI, C .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1989, 182 (03) :661-666
[9]   SYNTHESIS AND RELEASE OF PLATELET-ACTIVATING FACTOR IS INHIBITED BY PLASMA ALPHA-1-PROTEINASE INHIBITOR OR ALPHA-1-ANTICHYMOTRYPSIN AND IS STIMULATED BY PROTEINASES [J].
CAMUSSI, G ;
TETTA, C ;
BUSSOLINO, F ;
BAGLIONI, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 168 (04) :1293-1306
[10]  
CARELL RW, 1990, LUNG S, P530