Increased aryl hydrocarbon receptor expression in patients with allergic rhinitis.
BACKGROUND
A predominant Th17 population is a marker of allergic rhinitis (AR). As a ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR) plays a vital role in promoting or inhibiting the development of specific Th cells. However, its role in AR remains undefined.


OBJECTIVE
To analyze the potential role of AhR in the pathogenesis of AR.


METHODS
In total, 30 AR patients and 13 healthy controls were recruited for this study and AR patients had clinical features, as demonstrated by rhinoconjunctivitis quality of life questionnaires, total symptom scores and visual analog scale scores. The expression of AhR, IL-17 and IL-22 and the presence of Th17 cells in peripheral blood mononuclear cells were measured before and after treatment with the nontoxic AhR ligand 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE).


RESULTS
Pretreatment ITE studies revealed that all AR patients had a significant increase in AhR expression compared with controls and AhR expression positively correlated with clinical parameters. After ITE intervention, a severe reduction in the differentiation of Th17 cells and the production of IL-17 and IL-22 was noted in both AR patients and normal subjects. Simultaneously, a dramatic enhancement of AhR expression was also observed in all healthy controls, but not in AR patients.


CONCLUSIONS
The results suggested that the AhR may be one of the mechanisms underlying the Th17 response during the pathogenesis of AR and AhR levels were closely related to clinical severity in all AR patients. Additionally, ITE may represent a new drug candidate in the treatment of AR.
Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Yixueyuan Road, Chongqing, China 400016. hongsuling2013@yahoo.com.
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Wei
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Hu
H-Y
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Kang
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Yao
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Kou
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Liu
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Hong
D000328:Adult; D016022:Case-Control Studies; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D020381:Interleukin-17 / Q000096:biosynthesis; D007378:Interleukins / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics; D018336:Receptors, Aryl Hydrocarbon / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D065631:Rhinitis, Allergic; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology*; D012720:Severity of Illness Index; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D013844:Thiazoles / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects / Q000276:immunology; D055815:Young Adult; D000097043:Interleukin-22
D007211:Indoles; D020381:Interleukin-17; D007378:Interleukins; D012333:RNA, Messenger; D018336:Receptors, Aryl Hydrocarbon; D013844:Thiazoles; D000097043:Interleukin-22; C548651:2-(1'H-indole-3'-carbonyl)thiazole-4-carboxylic acid methyl ester