Journal
PHARMACOGENOMICS JOURNAL
Volume 6, Issue 2, Pages 141-152Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.tpj.6500357
Keywords
asthma; expression profiling; IL-13; allergen; lung; STAT6
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Funding
- NHLBI NIH HHS [U01HL66623, HL58527, HL10342] Funding Source: Medline
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Accumulating evidence in animal models and human asthma support a central role for IL-13 signaling in disease pathogenesis. In order to identify asthma and therapy associated genes, global transcriptional changes were monitored in mouse lung following antigen challenge (ovalbumin (OVA)), either alone or in the presence of a soluble IL-13 antagonist. Changes in whole lung gene expression after instillation of mIL-13 were also measured both in wild type and STAT6 deficient mice. A striking overlap in the gene expression profiles induced by either OVA challenge or mIL-13 was observed, further strengthening the relationship of IL-13 signaling to asthma. Consistent with results from functional studies, a subset of the OVA-induced gene expression was significantly inhibited by a soluble IL-13 antagonist while IL-13-modulated gene expression was completely attenuated in the absence of STAT6-mediated signaling. Results from these experiments greatly expand our understanding of asthma and provide novel molecular targets for therapy and potential biomarkers of IL-13 antagonism.
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