Abstract

Summary The functions of epithelial cells in the nose can be summarized as follows: (1) building a physical barrier to prevent allergens and foreign bodies from penetrating into the subepithelial layers; (2) secreting airway fluid by transepithelial ion transport and mucin production; and (3) responding to various stimuli by producing mediators that recruit lymphocytes, eosinophils, and mast cells to the nasal mucosa. However, in the setting of allergic rhinitis (AR) various morphological and functional changes occur in these cells, and the physical barrier of epithelial cells becomes vulnerable, which enables allergens to penetrate into the subepithelial layers. Histamine and thrombin are factors that influence the physical barrier. Although it is believed that epithelial damage in AR is less extensive than that in bronchial asthma, continued allergen exposure does damage epithelial cells in allergic animal models. Changes in ion transport during acute allergic reactions in vivo can be studied by nasal transepithelial potential difference. Comparison of nasal potential differences during pollen season has revealed lower values in allergic patients than in normal control subjects; the lowest value was reached 15 min after nasal allergen challenge. In vitro studies revealed that various factors including leukotrienes increase mucin gene transcription. These changes may lead to abnormalities of nasal secretion during allergic reactions.

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