LFA-1 expression by blood eosinophils is increased in atopic asthmatic children and is involved in eosinophil locomotion

Citation
S. Lantero et al., LFA-1 expression by blood eosinophils is increased in atopic asthmatic children and is involved in eosinophil locomotion, EUR RESP J, 12(5), 1998, pp. 1094-1098
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
EUROPEAN RESPIRATORY JOURNAL
ISSN journal
09031936 → ACNP
Volume
12
Issue
5
Year of publication
1998
Pages
1094 - 1098
Database
ISI
SICI code
0903-1936(199811)12:5<1094:LEBBEI>2.0.ZU;2-G
Abstract
Allergic asthma is characterized by eosinophil migration in the airways, wh ich is strictly dependent on the expression of adhession molecules. This st udy investigated whether the expression of adhesion molecules on eosinophil s is increased and associated with disease activity in allergic asthma, Twenty atopic asthmatic (AA) subjects and nine controls were studied and th e expression of lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18 ), Mac-1 (CD11b/CD18) and very late antigen-4 (VLA-4; CD49d/CD29) on blood eosinophils was evaluated by specific monoclonal antibody (Mab) staining an d flow-cytometric analysis. Compared with controls, eosinophils from AA showed increased expression of LFA-1 (p<0.005), but not of Mac-1 or VLA-4 (p>0.1). In addition, LFA-1 expr ession correlated positively with blood eosinophil number (r=0.792, p<0.05) , while no correlations were observed between Mac-1 or VLA-I expression and blood eosinophil number. The migration of eosinophils through human umbili cal vein endothelial cells with or without anti-LFA-1,Mac-1 and VLA-cl-bloc king Mab was studied. Compared with controls, eosinophils from AA showed in creased migration toward C5a (p<0.01), Cell migration was totally inhibited by preincubating eosinophils with anti-LFA-l (p<0.05), while anti-Mac-1 ha d no effect (p>0.1), Thus, the expression of lymphocyte function-associated antigen-1 by blood e osinophils is increased in atopic asthmatics and seems to modulate the enha nced eosinophil migration observed in allergic asthma.