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-Induced Fibroblasts
Department of Allergic Diseases, Novartis Research Institute, Vienna, Austria
Eosinophils are attracted to sites of allergic inflammation by a
number of chemoattractants including eotaxin-1. This chemokine can be
secreted from epithelial cells and fibroblasts after IL-4 and TNF-
stimulation in a synergistic fashion. TNF- activated gene expression
at the transcriptional level in a STAT6-dependent manner, because: 1)
eotaxin-1 promoter luciferase constructs were TNF- inducible in
STAT6-defective HEK293 cells only on cotransfection of STAT6 expression
vector, an effect that was partially mediated by activation-induced
binding of NF-
B proteins to a composite STAT6/NF-B element; 2)
reporter constructs defective in STAT6 DNA binding did not respond to
TNF- stimulation; 3) eotaxin-1 protein secretion was detected only
in STAT6-transfected HEK293 cell supernatants on TNF- treatment; and
4) a trans-dominant negative STAT6 protein inhibited
TNF--induced eotaxin-1 secretion in primary fibroblasts. TNF-
inducibility of the IL-8 and monocyte chemoattractant protein-1 genes
was not dependent on STAT6 expression in the same experimental systems.
The inducing effect of IL-4 and IL-13 was also mediated by STAT6. The
synergistic effect of IL-4 and TNF- observed at the RNA and the
protein level was not seen at the promoter level. The data demonstrate
that both IL-4 and TNF- induce eotaxin-1 expression at the level of
transcription via a STAT6-mediated pathway.
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