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Published ahead of print on February 14, 2003, doi:10.1165/rcmb.2002-0289OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 1, July 2003, 133-147

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Submitted on December 11, 2002
Revised on February 11, 2003

IL-3, 5 and GM-CSF-induced Adhesion Molecule Expression on Eosinophils by p38 MAPK and NF-{kappa}B

Chun K Wong1, Wai K Ip1, and Christopher W Lam1*

1 Chemical Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong

* To whom correspondence should be addressed. E-mail: waikeilam{at}cuhk.edu.hk.

We investigated the intracellular signaling mechanisms for cytokine IL-3, IL-5 or GM-CSF-induced expression of adhesion molecules including very late antigen 4 (CD49d), 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 NF-{kappa}B pathway was measured by flow cytometry and cDNA expression array, respectively. The phosphorylation of inhibitor kappa B-{alpha} and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot, whereas the NF-{kappa}B activity was measured by electrophoretic mobility shift assay. IL-3, IL-5 and GM-CSF could enhance p38 MAPK and NF-{kappa}B activity, and induce ICAM-1, CD11b and CD18 expressions on eosinophils. They could suppress ICAM-3 expression but had no effect on CD49d 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-{kappa}B activities, whereas the regulation of CD11b, CD18 and ICAM-3 expressions might be mediated through p38 MAPK but not NF-{kappa}B. These cytokines therefore play a crucial role, via the p38 MAPK and NF-{kappa}B pathways, in the expression of important adhesion molecules on eosinophils in allergic inflammation.




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