Rhinitis, sinusitis, and upper airway diseaseCigarette smoke combined with Toll-like receptor 3 signaling triggers exaggerated epithelial regulated upon activation, normal T-cell expressed and secreted/CCL5 expression in chronic rhinosinusitis
Section snippets
Methods
The study was approved by the Institutional Review Board of both Massachusetts General Hospital and the Massachusetts Eye and Ear Institute. Each subject gave informed consent and completed a questionnaire, allergy skin testing, and a rhinoscopic examination. Healthy controls (N = 9) included men and women between the ages of 21 and 70 years in good general health. Exclusion criteria included a history of smoking, nasal or sinus disease, use of nasal or sinus medications, asthma, allergic
Summary of subject characteristics
The demographics of the healthy controls (HCs) and subjects with CRS are summarized in Table I. HCs were younger (age, 28 ± 10.8 years vs CRS, 44 ± 7.4 years) but had a similar sex distribution (female:male ratio, 7:2 and 8:3, respectively). Four subjects with CRS had asthma. Positive allergy skin test results were found in 5 of 9 HCs (despite a negative history of allergic rhinitis) and 7 of 11 subjects with CRS. Serum cotinine (a metabolite of nicotine) levels averaged 0.07 ng/mL in HCs and
Discussion
In this study, we investigated the potential role of the sinonasal epithelium in the pathogenesis of CRS by examining inflammatory gene expression in PNEC cultures. We identified a mild increase in baseline epithelial expression of TNF-α and GRO-α in subjects with CRS. HCs and subjects with CRS responded similarly to CSE, TNF-α, LTA (TLR-2 stimulus), and LPS (TLR-4 stimulus) as well as CSE+LTA and CSE+LPS. dsRNA was the strongest stimulus of inflammatory gene expression. Furthermore, patients
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Supported by a grant from the Flight Attendants Medical Research Institute.
Disclosure of potential conflict of interest: D. L. Hamilos has received honoraria from Merck, Critical Therapeutics, Genentech, and Novartis; has consulting arrangements with GlaxoSmithKline, Novartis, Accentia, Schering-Plough, and Sinexus; has received research support from the Flight Attendants Medical Research Institute and Merck; and has received gifts from the GG Monks Foundation to purchase equipment. E. H. Holbrook has received research support from the National Institutes of Health-National Institutes of Deafness and Other Communication Disorders. S. T. Gray has served as a member of the American Academy of Otolaryngology and the American Rhinologic Society. N. Busaba is on the speakers' bureau for Sanofi-Aventis and Schering-Plough. The rest of the authors have declared that they have no conflict of interest.