title: Expression of prostaglandin E(2) receptor subtypes on cells in sputum from patients with asthma and controls: effect of allergen inhalational challenge.
abstract: BACKGROUND
  Prostaglandin (PG) E 2 binds to 4 G-protein-coupled receptors designated EP 1 through EP 4 . Although PGE 2 plays an immunomodulatory role in asthma, there is little information on the expression of PGE 2 receptors in this disease.
  
  
  OBJECTIVE
  We hypothesized that profiles of E-prostanoid (EP) receptor expression are altered on asthmatic bronchial inflammatory cells in vivo and further altered by allergen challenge in vivo and proinflammatory mediators in vitro.
  
  
  METHODS
  The numbers and phenotypes of EP 1-4 immunoreactive induced sputum cells from atopic asthmatics (n = 13; before and 24 hours after allergen inhalational challenge) and normal controls (n = 9; 3 after saline challenge) and EP 1-4 expression on purified blood eosinophils from both groups (n = 4 for each) before and after stimulation with LPS and/or IL-5 in vitro were measured by using single and double immunocytochemistry.
  
  
  RESULTS
  Subsets of sputum cells of all phenotypes expressed all 4 EP receptors in both patients with asthma and controls. There were significantly greater numbers of macrophages expressing all 4 EP receptors and increased percentages of macrophages expressing EP 2 and EP 4 in patients with asthma compared with controls. Allergen bronchial challenge of patients with asthma was associated with a selective influx of eosinophils, but the percentages of these and other leukocytes expressing all 4 EP receptors were unchanged. Compared with sputum, only small percentages of peripheral blood eosinophils expressed each receptor, but this was increased by culture with exogenous IL-5 or LPS.
  
  
  CONCLUSIONS
  E-prostanoid receptor expression is increased on airway macrophages of patients with asthma at baseline and may be altered on eosinophils after allergen challenge in vivo in response to inflammatory stimuli.
authors.affiliation: Department of Asthma, Allergy and Respiratory Science, Guy's King's and St Thomas' School of Medicine, London, UK. ying.sun@kcl.ac.uk
authors.forename: Sun
authors.initials: S
authors.lastname: Ying
authors.forename: Brian J
authors.initials: BJ
authors.lastname: O'Connor
authors.forename: Qiu
authors.initials: Q
authors.lastname: Meng
authors.forename: Natalie
authors.initials: N
authors.lastname: Woodman
authors.forename: Steven
authors.initials: S
authors.lastname: Greenaway
authors.forename: Helen
authors.initials: H
authors.lastname: Wong
authors.forename: Kirsty
authors.initials: K
authors.lastname: Mallett
authors.forename: Tak H
authors.initials: TH
authors.lastname: Lee
authors.forename: Chris
authors.initials: C
authors.lastname: Corrigan
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000276:immunology*; D001249:Asthma / Q000276:immunology / Q000378:metabolism*; D002452:Cell Count; D006801:Humans; D008168:Lung / Q000503:physiopathology; D018078:Receptors, Prostaglandin E / Q000145:classification*; D013183:Sputum / Q000737:chemistry* / Q000166:cytology
chemical_list: D000485:Allergens; D018078:Receptors, Prostaglandin E