No evidence for IgE receptor FcεRI expression on bronchial epithelial cells of asthmatic patients

Omer Qibi; Severine Audusseau; Andrea Mogas; Zoulfia Allakhverdi; Abdelilah Soussi Gounni; Saba Al Heialy; Qutayba Hamid; Omer Qibi; Severine Audusseau; Andrea Mogas; Zoulfia Allakhverdi; Abdelilah Soussi Gounni; Saba Al Heialy; Qutayba Hamid

doi:10.3934/Allergy.2018.4.165

AIMS Allergy and Immunology

2018, Volume 2, Issue 4: 165-179. doi: 10.3934/Allergy.2018.4.165

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Research article

No evidence for IgE receptor FcεRI expression on bronchial epithelial cells of asthmatic patients

1.
Meakins-Christie Laboratories, Research Institute of the McGill University Health Center, Montreal, Quebec, Canada
2.
Department of Immunology, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB
3.
MBRU, Dubai, United Arab Emirates
4.
College of Medicine, University of Sharjah, Sharjah, United Arab Emirates

Received: 10 August 2018 Accepted: 06 November 2018 Published: 12 November 2018

Immunoglobulin E (IgE) plays an important role in the pathogenesis of asthma and anti-IgE therapy was approved for treating patients with severe persistent allergic asthma. The exact target sites of anti-IgE therapy are not well characterized; however, it has been proposed that the therapeutic effects of anti-IgE come from its intervention in the airway remodeling process. To gain insights on how anti-IgE therapy improves asthma symptoms, we aimed to validate the expression of FcεRI on airway epithelial cells and demonstrate its role in airway remodeling. The expression of FcεRI was measured (1) in situ in bronchial biopsy tissues of asthmatic and control subjects using immunohistochemistry and (2) in vitro in primary bronchial epithelial cells obtained from asthmatic subjects, at baseline and after treatment with human IgE, using qPCR and flow cytometry. FcεRI expression in situ was detected only in a very small number of cells in the epithelium of bronchial biopsies of asthmatic and control subjects. In vitro measurement revealed no expression of the receptor both at baseline and after stimulation with IgE. The release of transforming growth factor—beta (TGF)-β and thymic stromal lymphopoietin (TSLP) were examined by ELISA in bronchial epithelial cells after crosslinking of IgE. No significant differences in TSLP and TGF-β protein levels were detected between stimulated and unstimulated cells. Hence, our data conclusively indicate that bronchial epithelial cells have negligible expression of functional high affinity receptor for IgE. Taken together, anti-IgE therapy is very likely to exert its therapeutic effects via other structural cell types.
- immunoglobulin E,
- high-affinity receptor FcεRI,
- severe asthma,
- airway inflammation,
- airway remodeling
Citation: Omer Qibi, Severine Audusseau, Andrea Mogas, Zoulfia Allakhverdi, Abdelilah Soussi Gounni, Saba Al Heialy, Qutayba Hamid. No evidence for IgE receptor FcεRI expression on bronchial epithelial cells of asthmatic patients[J]. AIMS Allergy and Immunology, 2018, 2(4): 165-179. doi: 10.3934/Allergy.2018.4.165

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Abstract

Immunoglobulin E (IgE) plays an important role in the pathogenesis of asthma and anti-IgE therapy was approved for treating patients with severe persistent allergic asthma. The exact target sites of anti-IgE therapy are not well characterized; however, it has been proposed that the therapeutic effects of anti-IgE come from its intervention in the airway remodeling process. To gain insights on how anti-IgE therapy improves asthma symptoms, we aimed to validate the expression of FcεRI on airway epithelial cells and demonstrate its role in airway remodeling. The expression of FcεRI was measured (1) in situ in bronchial biopsy tissues of asthmatic and control subjects using immunohistochemistry and (2) in vitro in primary bronchial epithelial cells obtained from asthmatic subjects, at baseline and after treatment with human IgE, using qPCR and flow cytometry. FcεRI expression in situ was detected only in a very small number of cells in the epithelium of bronchial biopsies of asthmatic and control subjects. In vitro measurement revealed no expression of the receptor both at baseline and after stimulation with IgE. The release of transforming growth factor—beta (TGF)-β and thymic stromal lymphopoietin (TSLP) were examined by ELISA in bronchial epithelial cells after crosslinking of IgE. No significant differences in TSLP and TGF-β protein levels were detected between stimulated and unstimulated cells. Hence, our data conclusively indicate that bronchial epithelial cells have negligible expression of functional high affinity receptor for IgE. Taken together, anti-IgE therapy is very likely to exert its therapeutic effects via other structural cell types.

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