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Clinical & Experimental Allergy

High expression of CD98 alters epithelial barrier functions to promote induction of airway allergy

Authors

  • T. Liu,

    Corresponding author
    • Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China
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    • These authors equally contributed to this work and are joint-first authors.
  • J. Ma,

    1. Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China
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    • These authors equally contributed to this work and are joint-first authors.
  • T.-L. Li,

    1. Department of Pathology & Molecular Medicine, McMaster University, Hamilton, ON, Canada
    2. Department of Otolaryngology, Shanxi Provincial People's Hospital, Taiyuan, China
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    • These authors equally contributed to this work and are joint-first authors.
  • J.-F. Yang,

    1. Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China
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  • X. Liang,

    1. Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China
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  • P.-C. Yang

    Corresponding author
    1. Department of Pathology & Molecular Medicine, McMaster University, Hamilton, ON, Canada
    • Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China
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Correspondence:

Dr T. Liu, Department of Otolaryngology, Head & Neck Surgery, the First Hospital, Shanxi Medical University, Taiyuan, China. E-mail: tao.liu43@yahoo.com

Dr P.-C. Yang, Room 3303, 50 Charlton Ave East, Hamilton, ON, Canada L8N 4A6. E-mail: yangp@mcmaster.ca

Summary

Background

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.

Objectives

This study aimed to investigate the role of overexpression of CD98 in the induction of nasal allergy.

Methods

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.

Results

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.

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