title: Enhanced expression of high-affinity IgE receptor (Fc epsilon RI) alpha chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells.
abstract: BACKGROUND
  IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (Fc epsilon RI) is involved in the pathogenesis of allergen-induced immediate and late responses.
  
  
  OBJECTIVE
  We investigated the expression and cellular distribution of Fc epsilon RI in the nasal mucosa after allergen challenge in patients with summer hay fever.
  
  
  METHODS
  Fourteen grass pollen-sensitive patients and seven normal control subjects underwent nasal challenge with grass pollen and allergen diluent in random order separated by 2 weeks. Nasal airway caliber was monitored by acoustic rhinometry, and nasal biopsy was performed at 6 hours. Messenger RNA for Fc epsilon RI was determined by using reverse-transcription polymerase chain reaction, and Fc epsilon RI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the alpha subunit. Co-localization of Fc epsilon RI receptors was performed by using double-immunostaining methods.
  
  
  RESULTS
  In atopic subjects, there was a significant early decrease in nasal airway caliber, which extended up to 6 hours after allergen challenge. Fc epsilon RI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing Fc epsilon RI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in Fc epsilon RI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of Fc epsilon RI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% Fc epsilon RI+ cells being unidentified.
  
  
  CONCLUSIONS
  Our results demonstrate increased Fc epsilon RI expression during allergen-induced rhinitis and highlight a potential target for treatment.
authors.affiliation: Upper Respiratory Medicine, Imperial College of Medicine, National Heart and Lung Institute, London, England.
authors.forename: K
authors.initials: K
authors.lastname: Rajakulasingam
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: F
authors.initials: F
authors.lastname: O'Brien
authors.forename: M
authors.initials: M
authors.lastname: Humbert
authors.forename: L T
authors.initials: LT
authors.lastname: Barata
authors.forename: L
authors.initials: L
authors.lastname: Reece
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
authors.forename: J A
authors.initials: JA
authors.lastname: Grant
mesh_terms: D000328:Adult; D000485:Allergens / Q000494:pharmacology*; D000915:Antibody Affinity; D002465:Cell Movement / Q000276:immunology; D003713:Dendritic Cells / Q000378:metabolism*; D004804:Eosinophils / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D008407:Mast Cells / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D017455:Receptors, IgE / Q000096:biosynthesis* / Q000235:genetics; D006255:Rhinitis, Allergic, Seasonal / Q000209:etiology / Q000276:immunology* / Q000378:metabolism
chemical_list: D000485:Allergens; D012333:RNA, Messenger; D017455:Receptors, IgE