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IL-9 induces VEGF secretion from human mast cells and IL-9/IL-9 receptor genes are overexpressed in atopic dermatitis.

Abstract
Interleukin 9 (IL-9) has been implicated in mast cell-related inflammatory diseases, such as asthma, where vascular endothelial growth factor (VEGF) is involved. Here we report that IL-9 (10-20 ng/ml) induces gene expression and secretion of VEGF from human LAD2. IL-9 does not induce mast cell degranulation or the release of other mediators (IL-1, IL-8, or TNF). VEGF production in response to IL-9 involves STAT-3 activation. The effect is inhibited (about 80%) by the STAT-3 inhibitor, Stattic. Gene-expression of IL-9 and IL-9 receptor is significantly increased in lesional skin areas of atopic dermatitis (AD) patients as compared to normal control skin, while serum IL-9 is not different from controls. These results imply that functional interactions between IL-9 and mast cells leading to VEGF release contribute to the initiation/propagation of the pathogenesis of AD, a skin inflammatory disease.
AuthorsNikolaos Sismanopoulos, Danae A Delivanis, Konstantinos D Alysandratos, Asimenia Angelidou, Magdalini Vasiadi, Anastasia Therianou, Theoharis C Theoharides
JournalPloS one (PLoS One) Vol. 7 Issue 3 Pg. e33271 ( 2012) ISSN: 1932-6203 [Electronic] United States
PMID22413008 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Chemical References
  • Interleukin-9
  • RNA, Messenger
  • Receptors, Interleukin-9
  • STAT3 Transcription Factor
  • Vascular Endothelial Growth Factor A
Topics
  • Cell Line
  • Dermatitis, Atopic (genetics, immunology, metabolism)
  • Humans
  • Interleukin-9 (blood, genetics, pharmacology)
  • Mast Cells (drug effects, immunology, metabolism)
  • Phosphorylation
  • RNA, Messenger (genetics, metabolism)
  • Receptors, Interleukin-9 (genetics)
  • STAT3 Transcription Factor (metabolism)
  • Vascular Endothelial Growth Factor A (metabolism)

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