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Interleukin-25 and Eosinophils Progenitor Cell Mobilization in Allergic Asthma
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A5952 - Interleukin-25 and Eosinophils Progenitor Cell Mobilization in Allergic Asthma
Author Block: W. Tang1, W. Du1, S. G. Smith2, R. Sehmi3, P. O'Byrne4; 1Pulmonary and Critical Care Medicine, Shanghai Ruijin Hospital affiliated to Shanghai Jiaotong University school of Medicine, Shanghai, China, 2GSK, Waterdown, ON, Canada, 3Medicine, McMaster University, Hamilton, ON, Canada, ON, Canada, 4Faculty Health Sciences, HSC, Rm 2E1, McMaster University, Hamilton, ON, Canada.
Introduction: Eosinophil progenitor cells play a role in allergic airway inflammation in asthma. Interleukin-25 is an epithelial derived cytokine, which is increased in plasma and whose receptor expression (IL-17RA, IL-17RB) is increased on eosinophils from allergic asthmatics after inhaled allergen. In this study, we examined the possible role of IL-25 on allergen-induced changes eosinophil progenitor cells in asthma. Methods: Asthmatics (n=14) who developed allergen-induced early and late responses were enrolled in a diluent-controlled allergen challenge cross-over study. Blood was collected at pre- and 24h post-challenge. Surface expression of IL-17RA, IL-17RB and intracellular IL-25 were evaluated by flow cytometry on eosinophil-lineage committed progenitors (EoP) chemotaxis. An in vitro migration assay was used to examine migrational responses of EoP. In addition, IL-25 knockout ovalbumin (OVA) sensitized and challenged mice were studied to evaluate in vivo mobilization effects of IL-25 on eosinophil and EoP. Results: There was a significant increase in numbers of EoP expressing IL-17RB 24h post-allergen inhalation challenge in allergic asthmatics, when compare to diluent inhalation. Pre-exposure to IL-25 primed the migrational responsiveness of EoP to stromal cell-derived factor (SDF)1α. In OVA sensitized mice, knocking out IL-25 significantly alleviated OVA-induced eosinophil infiltration in the airway, and newly produced eosinophils were reduced in both bone marrow and lung. Conclusions: These results suggest an important role for IL-25 in allergen-induced migration eosinophil progenitor cells into the airways
Author Block: W. Tang1, W. Du1, S. G. Smith2, R. Sehmi3, P. O'Byrne4; 1Pulmonary and Critical Care Medicine, Shanghai Ruijin Hospital affiliated to Shanghai Jiaotong University school of Medicine, Shanghai, China, 2GSK, Waterdown, ON, Canada, 3Medicine, McMaster University, Hamilton, ON, Canada, ON, Canada, 4Faculty Health Sciences, HSC, Rm 2E1, McMaster University, Hamilton, ON, Canada.
Introduction: Eosinophil progenitor cells play a role in allergic airway inflammation in asthma. Interleukin-25 is an epithelial derived cytokine, which is increased in plasma and whose receptor expression (IL-17RA, IL-17RB) is increased on eosinophils from allergic asthmatics after inhaled allergen. In this study, we examined the possible role of IL-25 on allergen-induced changes eosinophil progenitor cells in asthma. Methods: Asthmatics (n=14) who developed allergen-induced early and late responses were enrolled in a diluent-controlled allergen challenge cross-over study. Blood was collected at pre- and 24h post-challenge. Surface expression of IL-17RA, IL-17RB and intracellular IL-25 were evaluated by flow cytometry on eosinophil-lineage committed progenitors (EoP) chemotaxis. An in vitro migration assay was used to examine migrational responses of EoP. In addition, IL-25 knockout ovalbumin (OVA) sensitized and challenged mice were studied to evaluate in vivo mobilization effects of IL-25 on eosinophil and EoP. Results: There was a significant increase in numbers of EoP expressing IL-17RB 24h post-allergen inhalation challenge in allergic asthmatics, when compare to diluent inhalation. Pre-exposure to IL-25 primed the migrational responsiveness of EoP to stromal cell-derived factor (SDF)1α. In OVA sensitized mice, knocking out IL-25 significantly alleviated OVA-induced eosinophil infiltration in the airway, and newly produced eosinophils were reduced in both bone marrow and lung. Conclusions: These results suggest an important role for IL-25 in allergen-induced migration eosinophil progenitor cells into the airways
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