T sub(H)2 cytokines modulate the IL-9R expression on human neutrophils

Interleukin (IL)-9 is associated with key pathological features of asthma such as airway hyperresponsiveness, bronchoconstriction and mucus production. Inflammatory responses mediated by IL-9 rely on the expression of the IL-9R which has been reported on lung epithelial cells, T lymphocytes and rece...

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Published inBiochemical and biophysical research communications Vol. 384; no. 2; pp. 167 - 172
Main Authors Dragon, S, Takhar, M K, Shan, L, HayGlass, K T, Simons, F E, Gounni, A S
Format Journal Article
LanguageEnglish
Published 26.06.2009
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Abstract Interleukin (IL)-9 is associated with key pathological features of asthma such as airway hyperresponsiveness, bronchoconstriction and mucus production. Inflammatory responses mediated by IL-9 rely on the expression of the IL-9R which has been reported on lung epithelial cells, T lymphocytes and recently on airway granulocyte infiltrates. In this study, we assessed the regulatory and constitutive cell surface expression of the IL-9R alpha in unfractionated and purified human neutrophils from atopic asthmatics, atopic non-asthmatics and healthy normal controls. We demonstrate that T sub(H)2 cytokines (IL-4 or IL-13) and granulocyte macrophage-colony stimulating factor (GM-CSF) up-regulated mRNA and cell surface expression levels of the IL-9R alpha in primary human and HL-60 differentiated neutrophils. Pharmacological inhibition of NF- Kappa B did not affect T sub(H)2-mediated IL-9R alpha expression in human neutrophils although IFN- gamma and IL-10 down-regulated IL-9R alpha expression when co-incubated with IL-4, IL-13 or GM-CSF. Collectively, our results reveal a regulatory function for IFN- gamma and IL-10 on modulating the inducible IL-9R alpha expression levels on peripheral blood neutrophils by T sub(H)2 cytokines.
AbstractList Interleukin (IL)-9 is associated with key pathological features of asthma such as airway hyperresponsiveness, bronchoconstriction and mucus production. Inflammatory responses mediated by IL-9 rely on the expression of the IL-9R which has been reported on lung epithelial cells, T lymphocytes and recently on airway granulocyte infiltrates. In this study, we assessed the regulatory and constitutive cell surface expression of the IL-9R alpha in unfractionated and purified human neutrophils from atopic asthmatics, atopic non-asthmatics and healthy normal controls. We demonstrate that T sub(H)2 cytokines (IL-4 or IL-13) and granulocyte macrophage-colony stimulating factor (GM-CSF) up-regulated mRNA and cell surface expression levels of the IL-9R alpha in primary human and HL-60 differentiated neutrophils. Pharmacological inhibition of NF- Kappa B did not affect T sub(H)2-mediated IL-9R alpha expression in human neutrophils although IFN- gamma and IL-10 down-regulated IL-9R alpha expression when co-incubated with IL-4, IL-13 or GM-CSF. Collectively, our results reveal a regulatory function for IFN- gamma and IL-10 on modulating the inducible IL-9R alpha expression levels on peripheral blood neutrophils by T sub(H)2 cytokines.
Author Shan, L
Gounni, A S
HayGlass, K T
Takhar, M K
Simons, F E
Dragon, S
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