title: IL-25 and IL-25 receptor expression on eosinophils from subjects with allergic asthma.
abstract: BACKGROUND
  Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls.
  
  
  METHODS
  The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics.
  
  
  RESULTS
  The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003).
  
  
  CONCLUSIONS
  The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation.
authors.affiliation: Firestone Institute of Respiratory Health, Michael G DeGroote School of Medicine, McMaster University, Hamilton, Ont., Canada.
authors.forename: Wei
authors.initials: W
authors.lastname: Tang
authors.forename: Steven G
authors.initials: SG
authors.lastname: Smith
authors.forename: Sue
authors.initials: S
authors.lastname: Beaudin
authors.forename: Benny
authors.initials: B
authors.lastname: Dua
authors.forename: Karen
authors.initials: K
authors.lastname: Howie
authors.forename: Gail
authors.initials: G
authors.lastname: Gauvreau
authors.forename: Paul M
authors.initials: PM
authors.lastname: O'Byrne
mesh_terms: D000328:Adult; D001249:Asthma / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016022:Case-Control Studies; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015870:Gene Expression; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics* / Q000276:immunology; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D021122:Protein Subunits / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D053722:Receptors, Interleukin-17 / Q000235:genetics* / Q000276:immunology / Q000378:metabolism
chemical_list: C109985:IL17RA protein, human; D020381:Interleukin-17; D021122:Protein Subunits; D053722:Receptors, Interleukin-17