American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 146-153, (2002)
© 2002 American Thoracic Society
The Effects of Intranasal Budesonide on Allergen-induced Production of Interleukin-5 and Eotaxin, Airways, Blood, and Bone Marrow Eosinophilia, and Eosinophil Progenitor Expansion in Sensitized Mice
Huahao Shen,
Paul M. O'Byrne,
Russ Ellis,
Jennifer Wattie,
Chibing Tang and
Mark D. Inman
Asthma Research Group, Department of Medicine, McMaster University and St. Joseph's Hospital, Hamilton, Ontario, Canada; and Department of Respiratory Medicine, Second Hospital, Zhejiang University School of Medicine, Hangzhou, China
Correspondence and requests for reprints should be addressed to Dr. Mark D. Inman, Asthma Research Group, Firestone Regional Chest and Allergy Unit, Rm. 113, St. Joseph's Hospital, 500 Charlton Ave. E., Hamilton, Ontario, Canada L8N 4A6. E-mail: inmanma{at}fhs.mcmaster.ca
We have previously demonstrated that allergen inhalation induces expansion of bone marrow eosinophil progenitors in sensitized mice and subjects with asthma and that the inhaled corticosteroid, budesonide, reduced baseline but not allergen-induced increase in bone marrow eosinophil/basophil progenitors (EoB-CFU) in subjects with asthma. Here, we evaluated the effects of intranasal budesonide on allergen-induced increases in interleukin (IL)-5 and eotaxin in the airway and peripheral blood, expansion of bone marrow Eo-CFU and eosinophilia in bone marrow, peripheral blood and airway, as well as airway hyperresponsiveness, in ovalbumin (OVA)-sensitized mice. Budesonide treatment attenuated allergen-induced eosinophilia in bone marrow, peripheral blood, and airways as well as allergen-induced increases in bone marrow eosinophil progenitors but not allergen-induced increases in IL-5 or eotaxin 12 h following the second of two daily exposures to allergen; at later time points treatment was associated with attenuation of IL-5, eosinophilia, Eo-CFU, and airway hyperresponsiveness. These results suggest that a component of the mechanism by which corticosteroid treatment attenuates allergen-induced airway inflammation is through suppression of bone marrow eosinophilopoiesis, and that this is likely not mediated simply through the blocking of IL-5 production at the airway.
Key Words: corticosteroids • hemopoiesis • IL-5 • eosinophils • asthma
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Copyright © 2002 American Thoracic Society
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