MONOCYTE AND NEUTROPHIL ADHESION TO MATRIX PROTEINS IS SELECTIVELY ENHANCED IN THE PRESENCE OF INFLAMMATORY MEDIATORS

Citation
J. Lundahl et al., MONOCYTE AND NEUTROPHIL ADHESION TO MATRIX PROTEINS IS SELECTIVELY ENHANCED IN THE PRESENCE OF INFLAMMATORY MEDIATORS, Scandinavian journal of immunology, 44(2), 1996, pp. 143-149
Citations number
41
Categorie Soggetti
Immunology
ISSN journal
03009475
Volume
44
Issue
2
Year of publication
1996
Pages
143 - 149
Database
ISI
SICI code
0300-9475(1996)44:2<143:MANATM>2.0.ZU;2-6
Abstract
The authors investigated the time course of monocyte and neutrophil ad hesion to fibronectin, vitronectin and albumin precoated culture wells , using mixed leucocyte populations from healthy blood donors. Moreove r, the influence of chemotactic agonists on the adhesion properties as well as the quantitative expression of CD29, CD11b/CD18 and CD61 was analysed by flow cytometry. Different chemotactic agonists were used r epresenting a classical chemotactic agonist (fMLP), and agonists with a preferential effect on monocytes (RANTES) and neutrophils (IL-8), re spectively. The authors found a gradual increase in monocyte and neutr ophil adhesion to all three surfaces, reaching a plateau at 15 min of incubation. Adhesion to fibronectin was significantly higher at all ti me points (5, 15 and 60 min, respectively) compared with vitronectin a nd albumin in both monocytes and neutrophils. Neutrophil adhesion to v itronectin was significantly lower at 60 min compared with 15 min. Mon ocyte adhesion to albumin was increased by fMLP and RANTES and to vitr onectin also by IL-8. Neutrophil adhesion to albumin and vitronectin w as increased by fMLP and IL-8, but not RANTES. The adhesion to fibrone ctin was not altered by any of the chemotactic agonists used. The quan titative levels of CD11b/CD18, but not CD29 and CD61, was increased by fMLP, but not RANTES nor IL-8. The authors conclude that the adhesion of human monocytes and neutrophils to vitronectin and albumin, but no t fibronectin, is selectively enhanced by chemotactic agonists and may contribute to the selective accumulation of different leucocyte subse ts at the inflammatory site.