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Posters: Mechanisms of allergy

Background: In allergic inflammation, accumulation of eosinophils is mediated by selective adhesion and transmigration via the endothelium in the presence of eosinophil chemotactic factor (e.g. eotaxin) in the inflammatory sites. The adhesion of eosinophils to vascular endothelial cells can be enhanced by several cytokines, such as interferon g (IFN-g) and tumour necrosis factor-a (TNF-a), which have been shown to increase the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1) on the cells. However, the mechanisms by which regulating the expression of eosinophil adhesion molecules and related intracellular signal transduction are still unknown. Methods: We have studied the effect of TNF-a and how it regulate the expression of ICAM-1 on the human eosinophilic leukaemia cell line (EoL-1). In this study, the surface expression of ICAM-1 on EoL-1 was assessed by immunocytochemical staining. The phosphorylation of IkB-a and p38 MAPK was detected by Western blot. NF-kB pathway-related genes were evaluated by cDNA expression array system whereas the activity of NF-kB was accessed by electrophoretic mobility shift assay (EMSA). Results: It was demonstrated that TNF-a could up-regulate the surface expression of ICAM-1 in EoL-1 cells within 2 h. A specific proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132) but not a p38 MAPK inhibitor (SB 203580) was found to suppress the TNF-a-induced ICAM-1 expression on EoL-1 cells within 2 h. Using cDNA expression array, the gene expression of ICAM-1, NF-kB and IkB-a of the cells were up-regulated after 4 h treatment with TNF-a. Furthermore, TNF-a was shown to induce phosphorylation of IkB-a and p38 MAPK in EoL-1. The result of EMSA showed a band shifted on TNF-a-treated cells with or without p38 MAPK inhibitor, SB 203580. However, no shifted band was observed on MG-132treated EoL-1 cells. Conclusion: The activation of NF-kB but not p38 MAPK involved in the signalling pathways that control the expression of ICAM-1 for cell adhesion. Using this in vitro eosinophilic leukemic cell line, results further suggested the important role of NF-kB in recruitment of eosinophils in allergic inflammation.