title: Down-regulated IL-5 receptor expression on peripheral blood eosinophils from budesonide-treated children with asthma.
abstract: BACKGROUND
  The expression and function of cytokine receptors on peripheral blood eosinophils (PBE) from healthy and asthmatic children are poorly characterized.
  
  
  METHODS
  The PBE count and expression of IL-5 receptor (R) and GM-CSFR positive PBE was analyzed in nonsteroid-treated asthmatic children (n = 13), budesonide-treated asthmatic children (n = 24) and healthy children (n = 16) by flow cytometry. Alterations in intracellular EG2-epitope expression were used to measure the in vitro responsiveness of PBE to recombinant IL-5 and GM-CSF.
  
  
  RESULTS
  The PBE count was increased (P < 0.05) in both asthmatic groups, independent of treatment, as compared to healthy children. The IL-5R expression on PBE, as well as the in vitro responsiveness of PBE to recombinant IL-5, was reduced (P < 0.05), in budesonide-treated asthmatic children compared to nonsteroid-treated asthmatic children and healthy children. The proportion of GM-CSFR positive PBE and in vitro responsiveness of PBE to recombinant GM-CSF were not different between the groups. In vitro treatment with budesonide did not down-regulate the proportion of IL-5R positive PBE.
  
  
  CONCLUSIONS
  Budesonide-treatment of asthmatic children induces a selectively reduced IL-5R expression on PBE, concomitant with a reduced in vitro responsiveness of PBE to IL-5. We suggest that this budesonide-related down-regulation of the IL-5R might be a mechanism by which steroid treatment inhibits the action of IL-5 on eosinophil accumulation and activation in vivo.
authors.affiliation: Department of Medicine, Division of Clinical Immunology and Allergy, Stockholm, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Hellman
authors.forename: K
authors.initials: K
authors.lastname: Lönnkvist
authors.forename: G
authors.initials: G
authors.lastname: Hedlin
authors.forename: G
authors.initials: G
authors.lastname: Halldén
authors.forename: J
authors.initials: J
authors.lastname: Lundahl
mesh_terms: D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001249:Asthma / Q000097:blood* / Q000188:drug therapy*; D001798:Blood Proteins / Q000187:drug effects; D019819:Budesonide / Q000627:therapeutic use*; D002648:Child; D002669:Child Welfare; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000378:metabolism*; D000939:Epitopes / Q000187:drug effects; D005260:Female; D005541:Forced Expiratory Volume / Q000187:drug effects; D006801:Humans; D015848:Interleukin-5 / Q000097:blood / Q000502:physiology; D008297:Male; D011237:Predictive Value of Tests; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / Q000187:drug effects / Q000502:physiology; D018123:Receptors, Interleukin / Q000097:blood* / Q000502:physiology*; D053649:Receptors, Interleukin-5; D012260:Ribonucleases; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D000939:Epitopes; D015848:Interleukin-5; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5; D019819:Budesonide; D012260:Ribonucleases