Characterization of Interleukin-4–Stimulated nasal polyp fibroblasts

JW Steinke, CD Crouse, D Bradley, K Hise… - American journal of …, 2004 - atsjournals.org
JW Steinke, CD Crouse, D Bradley, K Hise, K Lynch, SE Kountakis, L Borish
American journal of respiratory cell and molecular biology, 2004atsjournals.org
Chronic hyperplastic eosinophilic sinusitis 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 interleukin (IL)-4 to fibroblast-mediated
inflammation in chronic hyperplastic eosinophilic sinusitis/NP. In addition, we hypothesized
that cysteinyl leukotrienes (CysLT) may directly influence fibroblast-mediated fibrotic and …
Chronic hyperplastic eosinophilic sinusitis 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 interleukin (IL)-4 to fibroblast-mediated inflammation in chronic hyperplastic eosinophilic sinusitis/NP. In addition, we hypothesized that cysteinyl leukotrienes (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 (transforming growth factor-β1 and -β2) and inflammatory cytokines and chemokines (IL-6 and CCL11) by fibroblasts as measured by semiquantitative and quantitative polymerase chain reaction, RNase protection assay, and enzyme-linked immunosorbent assay. The expression of CysLT and other proinflammatory 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 CysLT synthesis was not expressed in fibroblasts and could not be induced by IL-4 treatment.
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