title: Immuno-regulatory cytokines in asthma: IL-15 and IL-13 in induced sputum.
abstract: BACKGROUND
  The importance of Th2-type lymphocyte function in asthmatic airway inflammation is well recognized, but less is known about the factors which regulate the function of these lymphocytes in asthma. The macrophage-derived cytokine, interleukin (IL)-15 has a number of T cell regulatory properties which might be of relevance to asthma and its treatment.
  
  
  OBJECTIVE
  The aims were to identify and quantify the T cell regulatory cytokine IL-15 in induced sputum samples from asthmatic patients, in comparison with IL-13, and to relate the levels of these cytokines to treatment with inhaled steroids.
  
  
  METHODS
  Induced sputum was collected from 16 asthmatics (eight steroid and eight non-steroid treated) and eight normal controls. IL-15 and IL-13 levels were measured by enzyme-linked immunoassay (ELISA) in sputum. IL-15 levels were also measured in sputum cell culture supernatants and localized to specific sputum cells by immuno-cytochemistry.
  
  
  RESULTS
  IL-15 levels were increased and IL-13 levels were decreased in sputum fluid from steroid-treated compared with non-steroid-treated asthmatics. IL-15 was localized specifically to macrophages and the proportion of these cells expressing IL-15 correlated with sputum fluid IL-15 and IL-15 levels in cell culture supernatants, and all were higher in the steroid-treated asthmatics.
  
  
  CONCLUSIONS
  IL-15 and IL-13 production appears to be reciprocally regulated by steroid therapy in asthma patients. The steroid-associated increase in IL-15 may regulate a fundamental shift away from an inflammatory Th2-type environment in asthma and may be an essential component of the cytokine modulation underlying the therapeutic benefit of corticosteroids in this condition.
authors.affiliation: Department of Immunology, Western Infirmary, Glasgow, UK. mm6g@clin.med.gla.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Komai-Koma
authors.forename: A
authors.initials: A
authors.lastname: McKay
authors.forename: L
authors.initials: L
authors.lastname: Thomson
authors.forename: C
authors.initials: C
authors.lastname: McSharry
authors.forename: G W
authors.initials: GW
authors.lastname: Chalmers
authors.forename: F Y
authors.initials: FY
authors.lastname: Liew
authors.forename: N C
authors.initials: NC
authors.lastname: Thomson
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism*; D002478:Cells, Cultured / Q000737:chemistry / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000187:drug effects* / Q000502:physiology*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D018793:Interleukin-13 / Q000096:biosynthesis / Q000276:immunology / Q000378:metabolism; D019409:Interleukin-15 / Q000096:biosynthesis / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D013183:Sputum / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D013256:Steroids / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D018793:Interleukin-13; D019409:Interleukin-15; D013256:Steroids