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Allergic rhinitis is associated with decreased expression of Toll‐like receptor 9 by sinonasal epithelial cells
Author(s) -
Melvin ThuyAnh N.,
Nguyen MaiTien,
Lane Andrew P.,
Lin Sandra Y.
Publication year - 2011
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.20038
Subject(s) - tlr9 , medicine , innate immune system , immunology , receptor , toll like receptor , flow cytometry , chronic rhinosinusitis , cytokine , immune system , innate lymphoid cell , immunity , gene expression , biology , biochemistry , gene , dna methylation
Background Toll‐like receptors (TLRs) are important in sinonasal mucosal innate immunity. Previous studies demonstrate that sinonasal epithelial cell (SNEC) TLR9 expression is reduced in T‐helper 2 (Th2) cytokine‐predominant chronic rhinosinusitis with polyps, and with the in vitro application of Th2 cytokines. To further investigate in vivo modulation of TLR9 by the local cytokine environment, this study examines TLR9 expression in freshly isolated SNECs from subjects with and without active allergic rhinitis (AR). Methods SNECs were gathered via endoscopic‐guided middle meatal brushings from 9 AR subjects who were skin‐prick test (SPT)‐positive to environmental allergens in season at the time of study, and 8 controls. Flow cytometry was utilized to compare SNEC TLR9 expression in the 2 groups. Results TLR9 expression by SNEC in the AR group was significantly reduced compared to normals (35% ± 26% vs 76% ± 10%, p = 0.002). Conclusion Similar to observations in eosinophilic chronic rhinosinusitis, this study shows that active AR is associated with decreased SNEC TLR9 expression. These findings are consistent with the concept that Th2 cytokines suppress expression of TLR9 and other innate immune genes. Multiple endogenous and microbial factors likely modulate sinonasal innate immunity to maintain homeostasis and prevent infection in AR. © 2011 ARS‐AAOA, LLC.