Enhanced proteoglycan deposition in the airway wall of atopic asthmatics

被引:151
作者
Huang, J [1 ]
Olivenstein, R [1 ]
Taha, R [1 ]
Hamid, Q [1 ]
Ludwig, M [1 ]
机构
[1] McGill Univ, Meakins Christie Labs, Royal Victoria Hosp, Montreal, PQ H2X 2P2, Canada
关键词
D O I
10.1164/ajrccm.160.2.9809040
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Increased extracellular matrix (ECM) deposition in the airway wall contributes to the airway wall remodeling observed in asthmatics. Although alterations in collagen have been well described, less is known about changes in other components of the ECM, particularly proteoglycans (PGs). Endobronchial biopsies were obtained from seven patients with mild atopic asthma and six normal control subjects. Tissues were blocked in OCT and frozen in isopentane. Sections were immunostained with antibodies for the small leucine-rich PGs, lumican, biglycan, decorin, and fibromodulin and for versican, a large chondroitin sulfate PG. We calculated the area of positive staining in the subepithelial layer, correcting for basement membrane length. Lumican, biglycan, and versican were localized predominantly in the subepithelial layer of the airway wall in all groups. PG deposition was significantly increased in asthmatics as compared with that in control subjects. Furthermore, the degree of PG immunoreactivity was significantly correlated with airway responsiveness in the asthmatics (lumican; r = -0.77, p < 0.05; biglycan: r = -0.76, p < 0.05; versican: r = -0.74, p = 0.06). Our results suggest that PGs may play a role in airway wall remodeling and thereby, airway mechanics in asthma.
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页码:725 / 729
页数:5
相关论文
共 22 条
[11]  
HOLGATE ST, 1993, CHEST, V103, pS125
[12]   Matrix proteoglycans: From molecular design to cellular function [J].
Iozzo, RV .
ANNUAL REVIEW OF BIOCHEMISTRY, 1998, 67 :609-652
[13]   THE MECHANICS OF AIRWAY NARROWING IN ASTHMA [J].
JAMES, AL ;
PARE, PD ;
HOGG, JC .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 139 (01) :242-246
[14]   BRONCHIAL BIOPSIES IN ASTHMA - AN ULTRASTRUCTURAL, QUANTITATIVE STUDY AND CORRELATION WITH HYPERREACTIVITY [J].
JEFFERY, PK ;
WARDLAW, AJ ;
NELSON, FC ;
COLLINS, JV ;
KAY, AB .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 140 (06) :1745-1753
[15]  
LEBARON RG, 1992, J BIOL CHEM, V267, P10003
[16]   Eosinophil-associated TGF-beta(1) mRNA expression and airways fibrosis in bronchial asthma [J].
Minshall, EM ;
Leung, DYM ;
Martin, RJ ;
Song, YL ;
Cameron, L ;
Ernst, P ;
Hamid, Q .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1997, 17 (03) :326-333
[17]   EOSINOPHILS AS A POTENTIAL SOURCE OF PLATELET-DERIVED GROWTH-FACTOR B-CHAIN (PDGF-B) IN NASAL POLYPOSIS AND BRONCHIAL-ASTHMA [J].
OHNO, I ;
NITTA, Y ;
YAMAUCHI, K ;
HOSHI, H ;
HONMA, M ;
WOOLLEY, K ;
OBYRNE, P ;
DOLOVICH, J ;
JORDANA, M ;
TAMURA, G ;
TANNO, Y ;
SHIRATO, K .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 13 (06) :639-647
[18]   IS ASTHMA A FIBROTIC DISEASE [J].
ROBERTS, CR .
CHEST, 1995, 107 (03) :S111-S117
[19]  
Roberts CR., 1997, LUNG SCI FDN, P757
[20]  
ROCHE WR, 1989, LANCET, V1, P520