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Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Mucosal tissue polyclonal IgE is functional in response to allergen and SEB
N Zhang1, G Holtappels, P Gevaert
1Department of Oto-Rhino-Laryngology, Upper Airway Research Laboratory (URL), Ghent University Hospital, Ghent, Belgium. nan.zhang@ugent.be
Allergy
|July 28, 2010
Summary
In nasal polyp patients, local IgE antibodies are functional and activate mast cells, potentially driving chronic airway inflammation. This IgE presence in tissue may be independent of serum levels.
Area of Science:
- Immunology
- Otorhinolaryngology
- Allergy
Background:
- Staphylococcus aureus may influence airway diseases through local production of polyclonal IgE antibodies.
- The specific role of these IgE antibodies in airway disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate the presence and function of IgE antibodies in the nasal mucosa of patients with allergic rhinitis (AR) and nasal polyps (NP).
- To explore the relationship between local and systemic IgE levels and mast cell activation in these conditions.
Main Methods:
- Collected nasal mucosal tissue and serum from AR and NP patients.
- Assessed total and specific IgE levels against allergens and Staphylococcus aureus enterotoxin B.
- Stimulated tissue fragments and mast cell lines (RBL SX38) with various allergens and enterotoxin B.
Main Results:
- In AR patients, mast cell degranulation correlated with specific IgE presence and serum IgE levels.
- In NP patients, tissue mast cell activation correlated with local specific IgE, but not serum IgE. Tissue IgE was significantly higher than serum IgE.
- Functional IgE in NP tissue was demonstrated by its ability to degranulate mast cells.
Conclusions:
- Mucosal IgE antibodies in nasal polyps are functional and can activate mast cells.
- Specific IgE in nasal polyp tissue can exist independently of serum IgE.
- Superantigen-induced polyclonal IgE may contribute to chronic airway inflammation by sustained mast cell activation.
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