S Ying1, Q Meng, A B Kay, D S Robinson. 1. Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Faculty of Medicine, Imperial College, London, UK.
Abstract
BACKGROUND: Interleukin-9 is a T cell-derived Th2-type cytokine that has been linked to airway hyper-responsiveness, mucus hypersecretion and mast cell infiltration in animal models. We recently demonstrated the potential for IL-9 to act in human eosinophil development and survival. OBJECTIVES: The aims of this study were: (i) to compare IL-9 mRNA expression in bronchial biopsies between atopic asthmatics and normal controls, (ii) to investigate kinetic expression of IL-9 mRNA in skin biopsies after allergen challenge; and (iii) to relate IL-9 expression to infiltration of eosinophils, mast cell and T lymphocytes in local tissue. METHODS: Bronchial biopsies were obtained from atopic asthmatics (n = 12) and normal non-asthmatics (n = 12) at baseline. Skin biopsies were obtained from atopic subjects (n = 11) at 1, 3, 6, 24, 48 and 72 h after allergen challenge. Diluent challenge sites at 24 h were used as controls. IL-9 mRNA was identified using the technique of in situ hybridization. The numbers of eosinophils, mast cells and T cells were evaluated by immunohistochemistry. RESULTS: The numbers of IL-9 mRNA(+) cells present in the bronchial mucosa were significantly greater in atopic asthmatics than those in normal controls (P = 0.003). The numbers of eosinophils, but not mast cells, were also significantly higher in asthmatics (P < 0.005). The numbers of IL-9 mRNA(+) cells present in the airway of asthmatics significantly correlated with the numbers of eosinophils (r = 0.623, P = 0.03), but not mast cells or T cells. Compared with diluent challenge, the numbers of IL-9 mRNA(+) cells were significantly elevated at all allergen-challenged sites in the skin, with maximal signals at 48 h (P < 0.005). At 72 h, the numbers of IL-9 mRNA(+) cells significantly correlated with the numbers of eosinophils (r = 0.707, P = 0.015). CONCLUSION: Elevated expression of IL-9 in allergic inflammation may contribute to local eosinophil infiltration and survival in asthma and other allergic atopic diseases.
BACKGROUND:Interleukin-9 is a T cell-derived Th2-type cytokine that has been linked to airway hyper-responsiveness, mucus hypersecretion and mast cell infiltration in animal models. We recently demonstrated the potential for IL-9 to act in human eosinophil development and survival. OBJECTIVES: The aims of this study were: (i) to compare IL-9 mRNA expression in bronchial biopsies between atopic asthmatics and normal controls, (ii) to investigate kinetic expression of IL-9 mRNA in skin biopsies after allergen challenge; and (iii) to relate IL-9 expression to infiltration of eosinophils, mast cell and T lymphocytes in local tissue. METHODS: Bronchial biopsies were obtained from atopic asthmatics (n = 12) and normal non-asthmatics (n = 12) at baseline. Skin biopsies were obtained from atopic subjects (n = 11) at 1, 3, 6, 24, 48 and 72 h after allergen challenge. Diluent challenge sites at 24 h were used as controls. IL-9 mRNA was identified using the technique of in situ hybridization. The numbers of eosinophils, mast cells and T cells were evaluated by immunohistochemistry. RESULTS: The numbers of IL-9 mRNA(+) cells present in the bronchial mucosa were significantly greater in atopic asthmatics than those in normal controls (P = 0.003). The numbers of eosinophils, but not mast cells, were also significantly higher in asthmatics (P < 0.005). The numbers of IL-9 mRNA(+) cells present in the airway of asthmatics significantly correlated with the numbers of eosinophils (r = 0.623, P = 0.03), but not mast cells or T cells. Compared with diluent challenge, the numbers of IL-9 mRNA(+) cells were significantly elevated at all allergen-challenged sites in the skin, with maximal signals at 48 h (P < 0.005). At 72 h, the numbers of IL-9 mRNA(+) cells significantly correlated with the numbers of eosinophils (r = 0.707, P = 0.015). CONCLUSION: Elevated expression of IL-9 in allergic inflammation may contribute to local eosinophil infiltration and survival in asthma and other allergic atopic diseases.
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