These authors equally contributed to this work and are joint-first authors.
High expression of CD98 alters epithelial barrier functions to promote induction of airway allergy
Article first published online: 15 JUN 2012
© 2012 Blackwell Publishing Ltd
Clinical & Experimental Allergy
Volume 42, Issue 7, pages 1051–1059, July 2012
How to Cite
Cite this as: T. Liu, J. Ma, T.-L. Li, J.-F. Yang, X. Liang and P.-C. Yang, Clinical & Experimental Allergy, 2012 (42) 1051–1059.
- Issue published online: 15 JUN 2012
- Article first published online: 15 JUN 2012
- Accepted manuscript online: 9 FEB 2012 01:05PM EST
- Manuscript Accepted: 3 FEB 2012
- Manuscript Revised: 1 FEB 2012
- Manuscript Received: 29 OCT 2011
- Canadian Institutes of Health Research. Grant Numbers: 191063, 220058, 177843
- Natural Science & Engineering Research Council of Canada. Grant Number: 371268
- Shanxi Provincial Science Foundation
- epithelial barrier;
- nasal allergy;
- staphylococcal enterotoxin B
Epithelial barrier dysfunction is critical in the induction of allergy; the aetiology is to be further understood. A recent report indicates that CD98 plays a role in the intestinal epithelial barrier dysfunction.
This study aimed to investigate the role of overexpression of CD98 in the induction of nasal allergy.
The nasal epithelium samples were collected from 30 patients with allergic rhinitis and 30 healthy subjects. The contents of CD98 and Staphylococcal enterotoxin B (SEB) in the nasal epithelium samples were evaluated by using Western blotting. The effect of SEB of inducing the expression of CD98 was evaluated with an airway epithelial cell line, the 16HBE14o cells. The epithelial barrier function was assessed with the indicators of transepithelial resistance (TER) and permeability to horseradish peroxidase (HRP). A mouse model was employed to evaluate the role of CD98 in the induction of nasal allergy.
High levels of CD98 and SEB were detected in the nasal epithelium of patients with allergic rhinitis. A positive correlation was identified between CD98 and SEB in nasal epithelium samples. Exposure to SEB could induce the overexpression of CD98 in RPMI 2650 and 16HBE14o cells. The overexpression of CD98 down-regulated TER and increased the permeability to HRP in 16HBE14o monolayers. Concurrent exposure to SEB and OVA induced nasal allergies in a mouse model that could be blocked by pre-treatment with anti-CD98 antibody.
Conclusions and Clinical Relevance
CD98 plays a critical role in compromising the airway epithelial barrier function that contributes to the induction of airway allergy.