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Allergic rhinitis patients with recurrent acute sinusitis have increased sinonasal epithelial cell TLR9 expression
Author(s) -
Melvin ThuyAnh N.,
Lane Andrew P.,
Nguyen MaiTien,
Lin Sandra Y.
Publication year - 2010
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1016/j.otohns.2010.01.001
Subject(s) - sinusitis , tlr9 , medicine , innate immune system , allergy , immunology , immune system , meatus , flow cytometry , tlr2 , immunopathology , gastroenterology , gene expression , biology , surgery , biochemistry , dna methylation , gene
Objective Pilot study examining toll‐like receptor 9 (TLR9) expression by sinonasal epithelial cells in allergic rhinitis (AR) subjects with and without a history of recurrent acute rhinosinusitis (RARS). Study Design Cohort study. Setting Outpatient clinic. Subjects and Methods Adult subjects were eligible for study if skin tested positive for inhalant allergens, and positive allergens were in season at time of study. Subjects were considered to have AR+RARS if they had four symptomatic episodes with major/minor factors in 12 months and CT evidence of sinusitis. Eight AR‐only subjects and 13 AR+RARS subjects underwent endoscopic‐guided cell brushing from the middle meatus. Flow cytometry for TLR9 expression was performed on collected fresh sinonasal epithelial cells. Results The AR+RARS group was found to have a significant increase in TLR9 expression in the sinonasal epithelium (66% ± 30%) compared with that of AR‐only patients (32% ± 21%; P = 0.011). Conclusion The significant difference in expression of TLR9 in allergic sinusitis patients compared with allergy‐only patients in this study may indicate a difference in the role of innate immunity in these groups. The results suggest that expression of innate immune markers such as TLR9 may be upregulated in response to repeated microbial insults in AR+RARS. Further research is necessary to determine whether an initial impairment of innate immune gene expression may predispose some AR patients to subsequent development of RARS.

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