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Am. J. Respir. Crit. Care Med., Volume 164, Number 8, October 2001, 1403-1409

Interleukin-5 Induces CD34+ Eosinophil Progenitor Mobilization and Eosinophil CCR3 Expression in Asthma

ROBERT G. STIRLING, ELIZABETH L. J. VAN RENSEN, PETER J. BARNES, and K. FAN CHUNG

Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom; and Department of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands

Asthma is characterized by the accumulation of activated T cells and eosinophils within the airway. Eosinophils derive from CD34+ bone marrow progenitor cells under the influence of hematopoietic growth factors, subsequently migrating to the airways under the cooperative influence of interleukin (IL)-5 and chemokines, including eotaxin. We compared the relative effects of systemic versus local IL-5 on progenitor-cell mobilization and mature eosinophil phenotype by using flow cytometry, following the administration of intravenous (2 µg) or inhaled (15 µg) IL-5 to nine patients with mild asthma. Intravenous IL-5 induced a rapid reduction in circulating eosinophil counts followed by prolonged blood eosinophilia. Both intravenous (p < 0.002) and inhaled (p < 0.05) IL-5 significantly increased CD34+/CD45+ lymphoblastoid eosinophil progenitors. Intravenous IL-5 increased mature eosinophil CCR3 expression from a baseline mean fluorescence intensity (MFI) of 658 ± 51.7 to 995 ± 93.2 at 24 h (p < 0.05), but had no effect on interleukin-5 receptor subunit alpha  or CD11b expression. Lymphocyte CCR3 MFI was increased by intravenous IL-5 from 38.5 ± 13.6 at baseline to 73.6 ± 14.3 at 24 h (p < 0.05). Systemic IL-5 increased circulating eosinophil progenitors, suggesting a key role for systemic IL-5 in eosinophil mobilization. Further, IL-5 causes terminal maturation of the eosinophil by increasing CCR3 expression, potentially affecting CCR3-dependent chemotaxis by eosinophils and lymphocytes.




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