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.
Highlights
Interleukin 9 (IL-9) was first described in the late 1980s as a member of a growing number of cytokines that has pleiotropic functions in the immune system [1]
IL-9 stimulates vascular endothelial growth factor (VEGF) production in human mast cells To examine the effect of IL-9 on VEGF secretion, LAD2 cells were treated with IL-9 (10, 20 ng/ml) for 48 hr
We report here for the first time that IL-9 induces VEGF release from human mast cells
Summary
IL-9 was first described in the late 1980s as a member of a growing number of cytokines that has pleiotropic functions in the immune system [1]. IL-9 was initially purified and characterized as a T cell and mast cell growth factor [2]. TGF-beta and IL-4, that are secreted by mast cells, are potent cytokines in promoting the generation of IL-9secreting cells [3,8]. One of the main functions of IL-9 is to promote mast cell growth and function [9]. IL-9, alone or in combination with stem cell factor or FceRI, promotes the expression of mast cell proteases and pro-allergic cytokines in cultured mast cells [10,11,12]
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