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Published ahead of print on June 10, 2004, doi:10.1165/rcmb.2004-0089OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 3, September 2004, 283-291

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Submitted on March 15, 2004
Revised on June 9, 2004

Molecular Regulation of IL-13 and MCP-1 Expression in Human Mast Cells by IL-1{beta}

Steven A Lee1, S. Matthew Fitzgerald1*, Shau K Huang2, Chuanfu Li3, David S Chi1, and Guha Krishnaswamy1

1 Department of Internal Medicine, East Tennessee State University, Johnson City, Tennessee, USA, 2 Department of Surgery, East Tennessee State University, Johnson City, Tennessee, USA, 3 Asthma and Allergy Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

* To whom correspondence should be addressed. E-mail: mattfitzgerald1{at}aol.com.

Mast cells play pivotal roles in IgE-mediated airway inflammation, expressing interleukin-13 (IL-13) and monocyte chemoattracant protein-1 (MCP-1), which in turn regulate IgE synthesis and/or inflammatory cell recruitment. The molecular effects of interleukin-1 beta (IL-1{beta}) on cytokine expression by human mast cells have not been studied well. In this report, we provide evidence that human mast cells express the type 1 receptor for IL-1 (IL-1R1). We also demonstrate that IL-1{beta} and tumor necrosis factor alpha (TNF-{alpha}) are able to induce, individually or additively, dose-dependent expression of IL-13 and MCP-1 in these cells. The induction of IL-13 and MCP-1 gene expression by IL-1{beta} was accompanied by the activation of IL-1 receptor associated kinase (IRAK) and translocation of the transcription factor, nuclear factor kappaB (NF-{kappa}B) into the nucleus. Accordingly, Bay 11-7082, an inhibitor of NF-{kappa}B activation inhibited IL-1{beta}-induced IL-13 and MCP-1 expression. IL-1{beta} also induced IL-13 promoter activity, while enhancing the stability of IL-13 mRNA transcripts. Dexamethasone, a glucocorticoid, inhibited IL-1{beta}-induced nuclear translocation of NF-{kappa}B and also the secretion of IL-13 from mast cells. Our data suggests that IL-1{beta} can serve as a pivotal co-stimulus of inflammatory cytokine synthesis in human mast cells, and this may be partly mediated by IL-1 receptor-binding and subsequent signaling via nuclear translocation of NF-{kappa}B. IL-1{beta} being a ubiquitously expressed cytokine, these findings have important implications for non-IgE-mediated signaling in airway mast cells. This could have important implications for innate immunity and airway inflammatory responses, such as observed in extrinsic and intrinsic asthma.




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