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Published ahead of print on August 14, 2003, doi:10.1165/rcmb.2003-0071OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 2, February 2004, 212-219

A more recent version of this article appeared on February 1, 2004
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Submitted on March 6, 2003
Revised on August 13, 2003

Characterization of interleukin-4 stimulated nasal polyp fibroblasts

John W Steinke1*, Charles D Crouse2, Dewayne Bradley2, Kathleen Hise1, Kevin R Lynch3, Stilianos E Kountakis2, and Larry Borish1

1 Asthma and Allergic Disease Center, University of Virginia, Charlottesville, VA, USA, 2 Otolaryngology, University of Virginia, Charlottesville, VA, USA, 3 Pharmacology, University of Virginia, Charlottesville, VA, USA

* To whom correspondence should be addressed. E-mail: js3ch{at}virginia.edu.

Chronic hyperplastic eosinophilic sinusitis (CHS) is an inflammatory disease that results in the accumulation of eosinophils, fibroblasts, mast cells, and goblet cells at the site of injury. A common feature of this disease is the presence of nasal polyposis (NP). The current studies were designed to assess the contribution of IL-4 to fibroblast-mediated inflammation in CHS/NP. In addition, we hypothesized that CysLT may directly influence fibroblast-mediated fibrotic and remodeling pathways in this disorder. Fibroblasts were isolated from NP tissue. All fibroblast lines expressed the IL-4 receptor. IL-4 induced changes in mRNA and protein expression of fibrotic (TGF-{beta}1 and TGF-{beta}2) and inflammatory cytokines and chemokines (IL-6 and CCL11) by fibroblasts as measured by semi-quantitative and quantitative PCR, ribonuclease protection assay and ELISA. The expression of CysLT and other pro-inflammatory lipid receptors on fibroblasts was evaluated. CysLT1 and CysLT2 receptors were not expressed on fibroblasts however, LPA1 receptor was constitutively expressed and LPA2 receptor expression was upregulated by IL-4. The metabolic cascade involved in cysteinyl leukotriene synthesis was not expressed in fibroblasts and could not be induced by IL-4 treatment.




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