EOSINOPHIL INFILTRATION IS RELATED TO INCREASED EXPRESSION OF VASCULAR CELL-ADHESION MOLECULE-1 IN NASAL POLYPS

Citation
Fl. Jahnsen et al., EOSINOPHIL INFILTRATION IS RELATED TO INCREASED EXPRESSION OF VASCULAR CELL-ADHESION MOLECULE-1 IN NASAL POLYPS, American journal of respiratory cell and molecular biology, 12(6), 1995, pp. 624-632
Citations number
48
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
12
Issue
6
Year of publication
1995
Pages
624 - 632
Database
ISI
SICI code
1044-1549(1995)12:6<624:EIIRTI>2.0.ZU;2-N
Abstract
Endothelial adhesion molecules are important in the recruitment of leu kocytes to inflammatory sites. Nasal polyps characteristically contain a leukocyte infiltrate in which eosinophils often are remarkably prom inent. We have studied whether this feature is related to a particular profile of adhesion molecules on the local microvascular endothelium. Nasal polyps were obtained from 15 patients. Mucosal biopsy specimens of the lower and the middle turbinate from the same patients as well as from three control subjects served as reference tissue. Expression of endothelial adhesion molecules and the relative numbers of eosinoph ils and neutrophils were examined by two- and three-color immunofluore scence staining. Both the number of eosinophils and the proportion of vessels positive for vascular cell adhesion molecule-1 (VCAM-1) were s ignificantly increased in nasal polyps compared with the turbinate muc osa of the same patients (P = 0.008 and P = 0.001, respectively). By c ontrast, the number of neutrophils and the relative expression of E-se lectin and intercellular adhesion molecule-1 were similar at both tiss ue sites. Furthermore, the relative number of eosinophils in nasal pol yps was well correlated (r, = 0.73, P = 0.006) with the percentage of vessels positive for VCAM-1, but this was not true for neutrophils. Ta ken together, this direct in situ observation strongly supports the cr ucial role suggested for VCAM-1 in human eosinophil extravasation at i nflammatory sites.