INCREASED ADHESION TO VASCULAR CELL-ADHESION MOLECULE-1 AND INTERCELLULAR-ADHESION MOLECULE-1 OF EOSINOPHILS FROM PATIENTS WITH ASTHMA

Citation
L. Hakansson et al., INCREASED ADHESION TO VASCULAR CELL-ADHESION MOLECULE-1 AND INTERCELLULAR-ADHESION MOLECULE-1 OF EOSINOPHILS FROM PATIENTS WITH ASTHMA, Journal of allergy and clinical immunology, 96(6), 1995, pp. 941-950
Citations number
51
Categorie Soggetti
Immunology,Allergy
ISSN journal
00916749
Volume
96
Issue
6
Year of publication
1995
Part
1
Pages
941 - 950
Database
ISI
SICI code
0091-6749(1995)96:6<941:IATVCM>2.0.ZU;2-G
Abstract
Adhesion of peripheral blood eosinophil and neutrophil granulocytes to the endothelial cell adherence receptors E-selectin, vascular cell ad hesion molecule-1, and intercellular adhesion molecule-1 has been meas ured. The study included patients with allergic rhinitis, patients wit h mild allergic and nonallergic asthma, and healthy individuals; 10 pe rsons were in each group. In addition, assay of eosinophil and neutrop hil cell surface expression of the receptor complex CD11b/CD18 was per formed. Increased eosinophil adhesion to vascular cell adhesion molecu le-1 (p<0.05) and intercellular adhesion molecule-1 (p<0.05) was demon strated in the patients with a more labile asthma, that is, a peak exp iratory flow rate variability of more than 10%, suggesting a relations hip to the degree of ongoing inflammation in the airways of the patien ts. The increased eosinophil adhesion was most probably due to a funct ional upregulation of the CD11b/CD18 and very late activation antigen- 4 receptors, because the number of receptors measured as cell surface expression was unaltered. The increased eosinophil adhesion in the pat ients with high peak expiratory flow rate variability appeared indepen dent of atopy. The increased adhesion was not entirely specific to the eosinophils, because neutrophils from patients with a peak expiratory flow rate variability of more than 10% also demonstrated increased ad hesion to intercellular adhesion molecule-1 (p<0.05) when compared wit h neutrophils from the patients with low peak expiratory flow rate var iability. In conclusion, the demonstrated priming of eosinophil adhesi on to vascular cell adhesion molecule-1 and intercellular adhesion mol ecule-1 might be one contributing mechanism behind the selective accum ulation of eosinophils in the lung tissue of patients with asthma.