Abstract
BackgroundInterleukin 9 (IL-9) is produced by activated CD4+ T cells. Its effects include stimulation of mucus production, enhanced mast cell proliferation, enhanced eosinophil function, and IgE production. These effects are consistent with a role in allergic diseases. Glucocorticoids have potent anti-inflammatory effects, including suppression of cytokine synthesis, and are widely used in the treatment of allergic conditions.MethodsWe examined the effect of the glucocorticoid dexamethasone (Dex) on IL-9 mRNA expression and protein secretion with real-time RT-PCR and ELISA. Peripheral blood mononuclear cells (PBMC) were prepared from human volunteers and activated with OKT3. CD4+ T cells were purified from PBMC and activated with OKT3 plus PMA.ResultsIL-9 mRNA abundance and protein secretion were both markedly reduced following treatment of activated PBMC with Dex. mRNA levels were reduced to 0.7% of control values and protein secretion was reduced to 2.8% of controls. In CD4+ T cells, Dex reduced protein secretion to a similar extent. The IC50 value of Dex on mRNA expression was 4 nM.ConclusionThese results indicate that IL-9 production is very markedly inhibited by Dex. The findings raise the possibility that the beneficial effects of glucocorticoids in the treatment of allergic diseases are in part mediated by inhibition of IL-9 production.
Highlights
Interleukin 9 (IL-9) is produced by activated CD4+ T cells
Dexamethasone reduces IL-9 mRNA abundance In preliminary experiments, real-time RT-PCR revealed that OKT3 was a highly effective stimulus of IL-9 expression in Peripheral blood mononuclear cells (PBMC), as previously reported [2]
The effect of Dex on IL-9 mRNA abundance in PBMC was examined in 13 healthy individuals by real-time RT-PCR
Summary
Its effects include stimulation of mucus production, enhanced mast cell proliferation, enhanced eosinophil function, and IgE production. These effects are consistent with a role in allergic diseases. IL-9, which was first identified as a T cell growth factor [2], has multiple effects consistent with a role in allergic inflammation. IL-9 acts on the pulmonary epithelium to induce production of mucus [3] and chemokines [4]. It enhances eosinophil function via induction of the IL-5 receptor [5]. Mast cell numbers are elevated in the lung by IL-9 [7]
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