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.
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Authors | Nikolaos Sismanopoulos, Danae A Delivanis, Konstantinos D Alysandratos, Asimenia Angelidou, Magdalini Vasiadi, Anastasia Therianou, Theoharis C Theoharides |
Journal | PloS one
(PLoS One)
Vol. 7
Issue 3
Pg. e33271
( 2012)
ISSN: 1932-6203 [Electronic] United States |
PMID | 22413008
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Interleukin-9
- RNA, Messenger
- Receptors, Interleukin-9
- STAT3 Transcription Factor
- Vascular Endothelial Growth Factor A
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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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