Enhanced expression of high-affinity IgE receptor (FcεRI) α chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells

Karalasingam Rajakulasingam, Stephen R. Durham, Fiona O'Brien, Mark Humbert, Luis T. Barata, Lisa Reece, A. Barry Kay, J. Andrew Grant

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Background: IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (FcεRI) is involved in the pathogenesis of allergen-induced immediate and late responses. Objective: We investigated the expression and cellular distribution of FcεRI 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 FcεRI was determined by using reverse-transcription polymerase chain reaction, and FcεRI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the α subunit. Co-localization of FcεRI 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. FcεRI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing FcεRI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in FcεRI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of FcεRI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% FcεRI+ cells being unidentified. Conclusions: Our results demonstrate increased FcεRI expression during allergen-induced rhinitis and highlight a potential target for treatment.

Original languageEnglish (US)
Pages (from-to)78-86
Number of pages9
JournalJournal of Allergy and Clinical Immunology
Volume100
Issue number1
DOIs
StatePublished - 1997

Fingerprint

IgE Receptors
Rhinitis
Eosinophils
Mast Cells
Allergens
Dendritic Cells
Macrophages
Nose
Pollen
Poaceae
Acoustic Rhinometry
Messenger RNA
Seasonal Allergic Rhinitis
Basophils
Nasal Mucosa
Immunoglobulin E
Reverse Transcription
Proteins
Immunohistochemistry
Monoclonal Antibodies

Keywords

  • Allergic rhinitis
  • FcεRI receptors
  • IgE

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Enhanced expression of high-affinity IgE receptor (FcεRI) α chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells. / Rajakulasingam, Karalasingam; Durham, Stephen R.; O'Brien, Fiona; Humbert, Mark; Barata, Luis T.; Reece, Lisa; Kay, A. Barry; Grant, J. Andrew.

In: Journal of Allergy and Clinical Immunology, Vol. 100, No. 1, 1997, p. 78-86.

Research output: Contribution to journalArticle

Rajakulasingam, Karalasingam ; Durham, Stephen R. ; O'Brien, Fiona ; Humbert, Mark ; Barata, Luis T. ; Reece, Lisa ; Kay, A. Barry ; Grant, J. Andrew. / Enhanced expression of high-affinity IgE receptor (FcεRI) α chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells. In: Journal of Allergy and Clinical Immunology. 1997 ; Vol. 100, No. 1. pp. 78-86.
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abstract = "Background: IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (FcεRI) is involved in the pathogenesis of allergen-induced immediate and late responses. Objective: We investigated the expression and cellular distribution of FcεRI 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 FcεRI was determined by using reverse-transcription polymerase chain reaction, and FcεRI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the α subunit. Co-localization of FcεRI 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. FcεRI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing FcεRI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in FcεRI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of FcεRI+ cells were mast cells (64{\%}), followed by macrophages (20{\%}), eosinophils (4{\%}), and dendritic cells (2{\%}), with 10{\%} FcεRI+ cells being unidentified. Conclusions: Our results demonstrate increased FcεRI expression during allergen-induced rhinitis and highlight a potential target for treatment.",
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T1 - Enhanced expression of high-affinity IgE receptor (FcεRI) α chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells

AU - Rajakulasingam, Karalasingam

AU - Durham, Stephen R.

AU - O'Brien, Fiona

AU - Humbert, Mark

AU - Barata, Luis T.

AU - Reece, Lisa

AU - Kay, A. Barry

AU - Grant, J. Andrew

PY - 1997

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N2 - Background: IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (FcεRI) is involved in the pathogenesis of allergen-induced immediate and late responses. Objective: We investigated the expression and cellular distribution of FcεRI 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 FcεRI was determined by using reverse-transcription polymerase chain reaction, and FcεRI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the α subunit. Co-localization of FcεRI 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. FcεRI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing FcεRI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in FcεRI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of FcεRI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% FcεRI+ cells being unidentified. Conclusions: Our results demonstrate increased FcεRI expression during allergen-induced rhinitis and highlight a potential target for treatment.

AB - Background: IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (FcεRI) is involved in the pathogenesis of allergen-induced immediate and late responses. Objective: We investigated the expression and cellular distribution of FcεRI 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 FcεRI was determined by using reverse-transcription polymerase chain reaction, and FcεRI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the α subunit. Co-localization of FcεRI 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. FcεRI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing FcεRI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in FcεRI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of FcεRI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% FcεRI+ cells being unidentified. Conclusions: Our results demonstrate increased FcεRI expression during allergen-induced rhinitis and highlight a potential target for treatment.

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