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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.

AbstractBACKGROUND:
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.
AuthorsK Rajakulasingam, S R Durham, F O'Brien, M Humbert, L T Barata, L Reece, A B Kay, J A Grant
JournalThe Journal of allergy and clinical immunology (J Allergy Clin Immunol) Vol. 100 Issue 1 Pg. 78-86 (Jul 1997) ISSN: 0091-6749 [Print] United States
PMID9257791 (Publication Type: Clinical Trial, Journal Article, Randomized Controlled Trial)
Chemical References
  • Allergens
  • RNA, Messenger
  • Receptors, IgE
Topics
  • Adult
  • Allergens (pharmacology)
  • Antibody Affinity
  • Cell Movement (immunology)
  • Dendritic Cells (metabolism)
  • Eosinophils (metabolism)
  • Female
  • Humans
  • Immunohistochemistry
  • Macrophages (metabolism)
  • Male
  • Mast Cells (metabolism)
  • RNA, Messenger (biosynthesis)
  • Receptors, IgE (biosynthesis, genetics)
  • Rhinitis, Allergic, Seasonal (etiology, immunology, metabolism)

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