Am. J. Respir. Crit. Care Med., Volume 162, Number 6, December 2000, 2139-2144

The Effects of Inhaled Budesonide on Circulating Eosinophil Progenitors and Their Expression of Cytokines after Allergen Challenge in Subjects with Atopic Asthma

G. M. GAUVREAU, L. J. WOOD, R. SEHMI, R. M. WATSON, S. C. DORMAN, R. P. SCHLEIMER, J. A. DENBURG, and P. M. O'BYRNE

Asthma Research Group, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, Ontario, Canada; and Johns Hopkins Allergy and Asthma Research Center, Baltimore, Maryland

Allergen inhalation by dual responder subjects with atopic asthma is associated with an increase in circulating eosinophil/basophil colony-forming units (Eo/B CFU) and granulocyte-macrophage colony- stimulating factor (GM-CSF) immunolocalization in Eo/B colony cells grown in vitro. The current study examined the effect of the inhaled corticosteroid, budesonide, on the number of allergen- induced circulating eosinophils and Eo/B CFU, and immunolocalization of GM-CSF and interleukin-5 (IL-5) in Eo/B colony cells grown in vitro. Sixteen subjects with mild atopic asthma were treated for either 7 or 8 d with 200 µg inhaled budesonide or placebo twice a day. Peripheral blood was collected before and 24 h after allergen inhalation challenge and nonadherent mononuclear cells (NAMC) were grown in methylcellulose culture. Eo/B CFU were enumerated after 14 d in culture, and prepared on slides for immunocytochemistry. Budesonide attenuated the allergen-induced increase in circulating eosinophils (4.0 ± 0.4 × 10⁵/ml versus 6.5 ± 0.7 × 10⁵/ml, p = 0.0001), circulating Eo/B CFU (12.4 ± 2.3/10⁶ NAMC versus 18.8 ± 4.6/10⁶ NAMC, p = 0.05), and immunolocalization of GM-CSF in Eo/B colony cells (11.8 ± 1.9% positive versus 18.0 ± 2.2%, p = 0.01) but not immunolocalization of IL-5 (7.9 ± 1.4% versus 4.5 ± 0.6%, p > 0.05). Inhaled budesonide attenuated the number of allergen-induced circulating eosinophils and their progenitors grown in the presence of GM-CSF, which may partially be a result of regulating eosinophil progenitor expression of the autocrine growth factor GM-CSF.

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