Increased expression of the aryl hydrocarbon receptor in allergic nasal mucosa, contributing to chemokine secretion in nasal epithelium

Ha Kyun Kim, Jin Ho Kook, Ka Ram Kang, Dong Ju Oh, Tae-Hoon Kim, Sang Hag Lee

Research output: Contribution to journalArticle

Abstract

Background: Pollutants produced by industrial and traffic-related activities have been linked to allergic responses. These noxious agents induce their effects through the aryl hydrocarbon receptor (AhR). Objective: We analyzed the expression and distribution pattern of AhR in normal and allergic nasal mucosa, and cytokine-driven regulation of its expression. The production levels of chemokine in cultured nasal epithelial cells were evaluated after stimulation with AhR ligand. Methods: The expression levels and distribution pattern of AhR in normal, mild, and moderate-severe persistent allergic nasal mucosa were assessed by using real-time polymerase chain reaction, Western blot, and immunohistochemistry. The expression levels of AhR were determined in cultured nasal epithelial cells treated with T-helper 2 cytokines. In cultured epithelial cells stimulated with 2-(10H-indole-30-carbonyl)-thiazole-4-carboxylic acid methyl ester, the expression levels of granulocyte macrophage colony-stimulating factor, thymus and activation regulated chemokine, macrophage inflammatory protein 1, monocyte chemotactic protein 1, regulated on activation normal T-cell expressed and secreted, eotaxin, and interleukin 8 were measured with real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Results: Expression of AhR was observed in normal and allergic nasal mucosa where it is distributed in the epithelial layer, submucosal glands, endothelial cells, and inflammatory cells. Its expression levels are increased in allergic nasal mucosa and upregulated after stimulation with T-helper 2 cytokines. The stimulation with 2-(10H-indole-30-carbonyl)-thiazole-4-carboxylic acid methyl ester resulted in increased production of chemokines in cultured epithelial cells. Conclusion: Analysis of the study results indicated that increased expression levels of AhR may play a role in the pathogenesis of allergic rhinitis, which contributes to chemokine production in nasal mucosa.

Original languageEnglish
Pages (from-to)e107-e112
JournalAmerican Journal of Rhinology and Allergy
Volume30
Issue number4
DOIs
Publication statusPublished - 2016 Jul 1

Fingerprint

Aryl Hydrocarbon Receptors
Nasal Mucosa
Chemokines
Epithelial Cells
Thiazoles
Cytokines
Carboxylic Acids
Nose
Real-Time Polymerase Chain Reaction
Cultured Cells
Esters
Chemokine CCL17
Macrophage Inflammatory Proteins
Chemokine CCL2
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-8
Endothelial Cells
Western Blotting
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry

ASJC Scopus subject areas

  • Immunology and Allergy
  • Otorhinolaryngology

Cite this

Increased expression of the aryl hydrocarbon receptor in allergic nasal mucosa, contributing to chemokine secretion in nasal epithelium. / Kim, Ha Kyun; Kook, Jin Ho; Kang, Ka Ram; Oh, Dong Ju; Kim, Tae-Hoon; Lee, Sang Hag.

In: American Journal of Rhinology and Allergy, Vol. 30, No. 4, 01.07.2016, p. e107-e112.

Research output: Contribution to journalArticle

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abstract = "Background: Pollutants produced by industrial and traffic-related activities have been linked to allergic responses. These noxious agents induce their effects through the aryl hydrocarbon receptor (AhR). Objective: We analyzed the expression and distribution pattern of AhR in normal and allergic nasal mucosa, and cytokine-driven regulation of its expression. The production levels of chemokine in cultured nasal epithelial cells were evaluated after stimulation with AhR ligand. Methods: The expression levels and distribution pattern of AhR in normal, mild, and moderate-severe persistent allergic nasal mucosa were assessed by using real-time polymerase chain reaction, Western blot, and immunohistochemistry. The expression levels of AhR were determined in cultured nasal epithelial cells treated with T-helper 2 cytokines. In cultured epithelial cells stimulated with 2-(10H-indole-30-carbonyl)-thiazole-4-carboxylic acid methyl ester, the expression levels of granulocyte macrophage colony-stimulating factor, thymus and activation regulated chemokine, macrophage inflammatory protein 1, monocyte chemotactic protein 1, regulated on activation normal T-cell expressed and secreted, eotaxin, and interleukin 8 were measured with real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Results: Expression of AhR was observed in normal and allergic nasal mucosa where it is distributed in the epithelial layer, submucosal glands, endothelial cells, and inflammatory cells. Its expression levels are increased in allergic nasal mucosa and upregulated after stimulation with T-helper 2 cytokines. The stimulation with 2-(10H-indole-30-carbonyl)-thiazole-4-carboxylic acid methyl ester resulted in increased production of chemokines in cultured epithelial cells. Conclusion: Analysis of the study results indicated that increased expression levels of AhR may play a role in the pathogenesis of allergic rhinitis, which contributes to chemokine production in nasal mucosa.",
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