Background Basophils, together with mast cells and eosinophils, are effector cells most often associated with airway inflammation in patients with asthma and a marker of basophil activation and differentiation (CD203c) has been related to asthma exacerbation. Basophils can have also an important role in the initiation of Th2 inflammation, as these cells may be activated directly by tissue cytokines (IL-25, IL-33 and TSLP) released by epithelial cells in response to damage signals from allergens, bacterials, virus or pollutants. Airway epithelial damage is frequently observed in asthma and tissue cytokines have been reported to be overexpressed in bronchial biopsies of asthmatic patients. We investigated whether IL-25, IL-33 and TSLP receptors expression levels on basophil membrane are associated with the severity and control of asthma. Methods 20 patients with asthma (12 mild/moderate, 8 severe), 15 with eosinophilic and 5 with non eosinophilic asthma have been enrolled in the study. Basophils membrane expression of IL25 R, TSLP R and IL33 R was analyzed before and after IgE, fMLP, LPS, LTA-SA (Lipoteicoic Acid from S. Aureus) stimulation. Results TSLP R and IL25 R expression was significantly increased in eosinophilic compared to non-eosinophilic asthma at baseline (TSLP R: 5.4±3 vs 2.1±1.7, p=0.01; IL25 R: 13±6.7 vs 5.9±2.5, p=0.01) and after IgE stimulation (TSLP R: 5.9±2.7 vs 2.6±1.4, p=0.02; IL25 R: 34.2±15.5 vs 19.2±3.4, p=0.05). Atopy and severity of asthma were associated with lower ( 9.9±4.3 in atopic vs 18.1±7.3 non atopic, p=0.02) and higher (8.8±4.3 in mild/moderate vs 15.6±7.8 in severe, p=0.05) IL25 R expression respectively. IL33 R was not detectable. Conclusions The high expression of epithelial cytokines (IL-25 and TSLP) receptors on basophils of patients with eosinophilic asthma suggests the important role of tissue cytokines in driving Th2 immunity. Our data suggest that IL25R expression could be used as biomarker of asthma severity.
Basophils membrane expression of Th2 epithelial cytokines receptors in asthma: relationship with phenotype and severity
BOITA, MONICA;RAIE, ALBERTO;BUSSOLINO, Claudia;FORNERO, MONICA;BUCCA, Caterina;HEFFLER, Enrico Marco;ROLLA, Giovanni
2015-01-01
Abstract
Background Basophils, together with mast cells and eosinophils, are effector cells most often associated with airway inflammation in patients with asthma and a marker of basophil activation and differentiation (CD203c) has been related to asthma exacerbation. Basophils can have also an important role in the initiation of Th2 inflammation, as these cells may be activated directly by tissue cytokines (IL-25, IL-33 and TSLP) released by epithelial cells in response to damage signals from allergens, bacterials, virus or pollutants. Airway epithelial damage is frequently observed in asthma and tissue cytokines have been reported to be overexpressed in bronchial biopsies of asthmatic patients. We investigated whether IL-25, IL-33 and TSLP receptors expression levels on basophil membrane are associated with the severity and control of asthma. Methods 20 patients with asthma (12 mild/moderate, 8 severe), 15 with eosinophilic and 5 with non eosinophilic asthma have been enrolled in the study. Basophils membrane expression of IL25 R, TSLP R and IL33 R was analyzed before and after IgE, fMLP, LPS, LTA-SA (Lipoteicoic Acid from S. Aureus) stimulation. Results TSLP R and IL25 R expression was significantly increased in eosinophilic compared to non-eosinophilic asthma at baseline (TSLP R: 5.4±3 vs 2.1±1.7, p=0.01; IL25 R: 13±6.7 vs 5.9±2.5, p=0.01) and after IgE stimulation (TSLP R: 5.9±2.7 vs 2.6±1.4, p=0.02; IL25 R: 34.2±15.5 vs 19.2±3.4, p=0.05). Atopy and severity of asthma were associated with lower ( 9.9±4.3 in atopic vs 18.1±7.3 non atopic, p=0.02) and higher (8.8±4.3 in mild/moderate vs 15.6±7.8 in severe, p=0.05) IL25 R expression respectively. IL33 R was not detectable. Conclusions The high expression of epithelial cytokines (IL-25 and TSLP) receptors on basophils of patients with eosinophilic asthma suggests the important role of tissue cytokines in driving Th2 immunity. Our data suggest that IL25R expression could be used as biomarker of asthma severity.
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