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Interleukin-3, -5, and Granulocyte Macrophage Colony-Stimulating Factor–Induced Adhesion Molecule Expression on Eosinophils by p38 Mitogen-Activated Protein Kinase and Nuclear Factor-B

Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong

Address correspondence to: Professor C. W. K. Lam, Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong. E-mail: waikeilam{at}cuhk.edu.hk

We investigated the intracellular signaling mechanisms for cytokine interleukin (IL)-3, IL-5, or granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced expression of adhesion molecules including very late antigen 4 (CD49 d), macrophage antigen-1 (CD11b), leukocyte function–associated antigen-1 (CD11a/CD18), intercellular adhesion molecule (ICAM)-1, and ICAM-3 on eosinophils. The expression of adhesion molecules and nuclear factor (NF)-B pathway was measured by flow cytometry and cDNA expression array, respectively. The phosphorylation of inhibitor B- and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot, whereas NF-B activity was measured by electrophoretic mobility shift assay. IL-3, IL-5, and GM-CSF could enhance p38 MAPK and NF-B activity and induce ICAM-1, CD11b, and CD18 expressions on eosinophils. They could suppress ICAM-3 expression, but had no effect on CD49 d expression. Either SB 203580 or MG-132 was able to offset the cytokine-induced expression of ICAM-1. Only SB 203580 could reverse the effect on CD11b, CD18, and ICAM-3 expressions. Therefore, the expression of ICAM-1 might involve both p38 MAPK and NF-B activities, whereas the regulation of CD11b, CD18, and ICAM-3 expressions might be mediated through p38 MAPK but not NF-B. These cytokines therefore play a crucial role, via the p38 MAPK and NF-B pathways, in the expression of important adhesion molecules on eosinophils in allergic inflammation.

Abbreviations: dimethyl sulfoxide, DMSO • eosinophilic cationic protein, ECP • electrophoretic mobility shift assay, EMSA • fluorescein isothiocyanate, FITC • granulocyte macrophage colony-stimulating factor, GM-CSF • inhibitor B-, IB- • intercellular adhesion molecule, ICAM • immunoglobulin, Ig • interleukin, IL • leukocyte function-associated antigen, LFA • lipopolysaccharide, LPS • macrophage antigen-1, Mac-1 • mitogen-activated protein kinase, MAPK • monocyte chemotactic protein, MCP • macrophage inflammatory protein, MIP • nuclear factor-B, NF-B • phosphate-buffered saline, PBS • tumor necrosis factor-, TNF- • vascular cell adhesion molecule, VCAM • very late antigen-4, VLA-4

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