Interleukin-5 enhances the in vitro adhesion of human eosinophils, but not neutrophils, in a leucocyte integrin (CD11/18)-dependent manner

• Published in: International archives of allergy and applied immunology Vol. 94; no. 1-4; p. 174
• Main Authors: Walsh, G M, Wardlaw, A J, Hartnell, A, Sanderson, C J, Kay, A B
• Format: Journal Article
• Language: English
• Published: Switzerland 1991
• Subjects: Antigens, CD - physiology; CD11 Antigens; CD18 Antigens; Cell Adhesion - drug effects; Cells, Cultured; Eosinophils - drug effects; Eosinophils - physiology; Humans; Interleukin-5 - pharmacology; Lymphocyte Function-Associated Antigen-1 - analysis; Macrophage-1 Antigen - analysis; Neutrophils - drug effects; Neutrophils - physiology
• ISSN: 0020-5915
• DOI: 10.1159/000235355

Interleukin (IL-5) was found to enhance the adhesion of eosinophils, but not neutrophils, to both microvascular and large vein endothelial cells in a dose-dependent manner. Granulocyte/macrophage-colony-stimulating factor (GM-CSF) and platelet-activating factor (PAF) enhanced both eosinophil and neutrophil adhesion. Significant increases in eosinophil CR3 expression, but not LFA-1, were observed following pre-incubation with PAF, IL-3, IL-5 or GM-CSF. Neutrophil CR3 expression was increased significantly by pre-incubation with PAF or GM-CSF, but not IL-3 or IL-5. Enhanced adhesion to human microvascular endothelial cells (HMVEC) or human umbilical vein endothelial cells (HUVEC) was inhibited by (ranked in order of potency) anti-CR3 alpha = common beta-chain greater than LFA-1 alpha. Anti-p150,95 alpha had no measurable effect. Basal expression of eosinophil CR3 with monoclonal antibody inhibited IL-5-induced eosinophil hyperadherence to HUVEC in a manner almost identical to inhibition in the presence of excess anti-CR3. Thus, a conformational or affinity change in adhesion receptors following activation seems more important than a simple increase in numbers. No inhibition of unstimulated eosinophil adhesion to HMVEC or HUVEC by CD11/18 monoclonal antibody was observed. These findings demonstrate that IL-5 enhances eosinophil, but not neutrophil, adherence reactions, by a mechanism dependent, at least in part, on the CD11/18 family of adhesion glycoproteins.