FUNCTIONAL-CHARACTERISTICS OF BRONCHIAL EPITHELIUM OBTAINED BY BRUSHING FROM ASTHMATIC AND NORMAL SUBJECTS

被引:83
作者
CAMPBELL, AM
CHANEZ, P
VIGNOLA, AM
BOUSQUET, J
COURET, I
MICHEL, FB
GODARD, P
机构
[1] Service des Maladies Respiratoires, Hopital Aiguelongue, 34059 Montpellier-Cedex, Avenue du Major Flandre
来源
AMERICAN REVIEW OF RESPIRATORY DISEASE | 1993年 / 147卷 / 03期
关键词
D O I
10.1164/ajrccm/147.3.529
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Airways epithelial cells may be involved in the pathogenesis of asthma, but their role remains to be determined. Epithelial cells can release large amounts of 15-hydroxyeicosatetranoic acid (15-HETE) and smaller amounts of prostaglandin E2 (PGE2) as well as fibronectin, a mediator involved in epithelial repair after injury. Epithelial cells obtained after bronchial brushing of 16 asthmatic (age 38 +/- 5 yr) and 11 normal subjects (age 36 +/- 5 yr) were studied. The percentage of epithelial cells was assessed by immunocytochemistry using an anti-cytokeratin antibody. The viability of the cells was assessed by trypan blue exclusion. The release of 15-HETE PGE2 and fibronectin was studied in resting cells and after A23187 calcium ionophore stimulation. Epithelial cells always comprised more than 86% of cells recovered, and the viability of epithelial cells was significantly (p < 0,001, Mann-Whitney U test) greater in normal subjects (54 +/- 5%) compared with asthmatic subjects (13 +/- 1%). The release of 15-HETE and fibronectin by resting epithelial cells was significantly greater in asthmatics (p < 0.05, Mann-Whitney U test) than in normal subjects. A23187 significantly (p < 0.05, Wilcoxon W test) increased the release of 15-HETE and fibronectin. There was no significant difference in the release of PGE2 by resting cells from either asthmatics or normal subjects, but challenge with A23187 induced a significant (p < 0.03, Wilcoxon W test) increase in PGE2 from cells of asthmatics but not from cells of normal subjects. This study shows that epithelial cells are activated and less viable in asthma and suggests a role for these cells in asthma.
引用
收藏
页码:529 / 534
页数:6
相关论文
共 35 条
[2]   INTEGRINS AND OTHER CELL-ADHESION MOLECULES [J].
ALBELDA, SM ;
BUCK, CA .
FASEB JOURNAL, 1990, 4 (11) :2868-2880
[3]   CELLULAR EVENTS IN THE BRONCHI IN MILD ASTHMA AND AFTER BRONCHIAL PROVOCATION [J].
BEASLEY, R ;
ROCHE, WR ;
ROBERTS, JA ;
HOLGATE, ST .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 139 (03) :806-817
[4]   EOSINOPHILIC INFLAMMATION IN ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
BARNEON, G ;
GHAVANIAN, N ;
ENANDER, I ;
VENGE, P ;
AHLSTEDT, S ;
SIMONYLAFONTAINE, J ;
GODARD, P ;
MICHEL, FB .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (15) :1033-1039
[5]  
CASALE TB, IMMUNOLOGY LUNG UPPE, P326
[6]  
CHANEZ P, 1989, American Review of Respiratory Disease, V139, pA482
[7]   ENHANCED ALVEOLAR CELL LUMINOL-DEPENDENT CHEMILUMINESCENCE IN ASTHMA [J].
CLUZEL, M ;
DAMON, M ;
CHANEZ, P ;
BOUSQUET, J ;
DEPAULET, AC ;
MICHEL, FB ;
GODARD, P .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1987, 80 (02) :195-201
[8]   IMMUNOENZYMATIC LABELING OF MONOCLONAL-ANTIBODIES USING IMMUNE-COMPLEXES OF ALKALINE-PHOSPHATASE AND MONOCLONAL ANTI-ALKALINE PHOSPHATASE (APAAP COMPLEXES) [J].
CORDELL, JL ;
FALINI, B ;
ERBER, WN ;
GHOSH, AK ;
ABDULAZIZ, Z ;
MACDONALD, S ;
PULFORD, KAF ;
STEIN, H ;
MASON, DY .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1984, 32 (02) :219-229
[9]  
DAVIES R J, 1990, Journal of Allergy and Clinical Immunology, V85, P155
[10]  
ELLIS AG, 1906, AM J MED SCI, V136, P407