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Interleukin-25–Induced Chemokines and Interleukin-6 Release from Eosinophils Is Mediated by p38 Mitogen-Activated Protein Kinase, c-Jun N-Terminal Kinase, and Nuclear Factor-B

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

Correspondence and requests for reprints should be addressed to Professor C. W. K. Lam, Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong. E-mail: waikeilam{at}cuhk.edu.hk

Interleukin (IL)-25, a novel Th2 cytokine, is capable of amplifying allergic inflammation. We investigated the modulation of nuclear factor (NF)-B and mitogen-activated protein kinases (MAPK) pathways in IL-25–activated eosinophils, the principal effector cells of allergic inflammation, for the in vitro release of chemokines including monocyte chemoattractant protein-1 (MCP-1), IL-8, and macrophage inflammatory protein (MIP)-1, and inflammatory cytokine IL-6. Gene expression of chemokines and IL-6 was evaluated by RT-PCR, and concentrations of chemokines and cytokine were measured by cytokine protein array, cytometric bead array, and enzyme-linked immunosorbent assay. NF-B, c-Jun amino-terminal kinase (JNK), and p38 MAPK activities in eosinophils were assessed by electrophoretic mobility shift assay and Western blot. IL-25 was found to upregulate the gene expression of chemokines MCP-1, MIP-1, and IL-8, and cytokine IL-6, in eosinophils, and to significantly increase the release of the above chemokines and IL-6 from eosinophils. IL-25 could also activate the JNK, p38 MAPK, and NF-B activities of eosinophils, while inhibitor of IB- phosphorylation (BAY11–7082), JNK (SP600125), and p38 MAPK (SB203580) could suppress the release of IL-8, MIP-1, MCP-1, and IL-6. Together, the above results showed that the induction of MCP-1, MIP-1, IL-8, and IL-6 in IL-25–activated eosinophils are regulated by JNK, p38 MAPK, and NF-B pathways.

Key Words: chemokines • eosinophils • interleukin-25 • mitogen-activated protein kinase • nuclear factor-B

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