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International Immunology Advance Access originally published online on October 21, 2008
International Immunology 2008 20(12):1565-1573; doi:10.1093/intimm/dxn115
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

IL-18 induces a marked gene expression profile change and increased Ccl1 (I-309) production in mouse mucosal mast cell homologs

Zoltan Wiener1, Peter Pocza1, Melinda Racz1, Gyorgy Nagy1, Gergely Tolgyesi1, Viktor Molnar1, Judit Jaeger2, Edit Buzas1, Eva Gorbe2, Zoltan Papp2, Janos Rigo2 and Andras Falus1,3

1 Department of Genetics, Cell and Immunobiology, Semmelweis University, H-1089 Budapest, Nagyvarad ter 4, Hungary
2 First Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary
3 Inflammation Biology and Immunogenomics Research Group, Hungarian Academy of Sciences, Budapest, Hungary

Correspondence to: A. Falus; E-mail: faland{at}dgci.sote.hu

Helminthic infections, which are particularly common in the developing world, are associated with the accumulation of mucosal mast cells (MMCs) in the epithelial layer of the gut. Although intestinal parasite infection models argue that IL-18 plays a role in MMC differentiation and function, the direct effect of IL-18 on MMCs is still not well understood. To clarify the role of IL-18 in mast cell biology, we analyzed gene expression changes in MMCs in vitro. DNA microarray technology uncovered a group of chemokines regulated by IL-18, among which Ccl1 (I-309, TCA-3) showed the highest up-regulation. Ccl1 induction was only transient in mast cells and was characteristic for both immature and mature MMCs, but not for connective tissue-type mast cells. IL-18 exerts its Ccl1-inducing effect in MMCs primarily via the activation of NF{kappa}B. Moreover, IL-18 was effective both in the absence and the presence of IgE–antigen complex. The Ccl1 receptor (CCR8) is known to be expressed by Th2 cells and is involved in their recruitment. Our present findings suggest that IL-18 may contribute to mast cell-influenced Th2 responses by inducing Ccl1 production.

Keywords: Ccl1, IgE/antigen, mast cell, microarray, NF{kappa}B, nitric oxide

Transmitting editor: I. Pecht

Received 11 June 2008, accepted 25 September 2008.


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