ArticleInternational forum of allergy & rhinology2017
Denatonium-induced sinonasal bacterial killing may play a role in chronic rhinosinusitis outcomes.
Article in International forum of allergy & rhinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Taste receptors in chronic rhinosinusitus, what is the evidence? A systematic review.International forum of allergy & rhinology · 2022Pooled it
- Trial
- A Review on the Nasal Microbiome and Various Disease Conditions for Newer Approaches to Treatments.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2023Article
- Pharmacology of T2R Mediated Host-Microbe Interactions.Handbook of experimental pharmacology · 2022Article
- Bitter Taste Receptor T2R14 Modulates Gram-Positive Bacterial Internalization and Survival in Gingival Epithelial Cells.International journal of molecular sciences · 2021Article
- Divergent bitter and sweet taste perception intensity in chronic rhinosinusitis patients.International forum of allergy & rhinology · 2021Article
- Tuft cells in the pathogenesis of chronic rhinosinusitis with nasal polyps and asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2021Review
- The microbiome of the upper respiratory tract in health and disease.BMC biology · 2019Review
- Gingival solitary chemosensory cells are immune sentinels for periodontitis.Nature communications · 2019Article
- Taste Receptors in Upper Airway Innate Immunity.Nutrients · 2019Review
- Species-level bacterial community profiling of the healthy sinonasal microbiome using Pacific Biosciences sequencing of full-length 16S rRNA genes.Microbiome · 2018Article
- The Role of Quinine-Responsive Taste Receptor Family 2 in Airway Immune Defense and Chronic Rhinosinusitis.Frontiers in immunology · 2018Article
- Taste Receptor Polymorphisms and Immune Response: A Review of Receptor Genotypic-Phenotypic Variations and Their Relevance to Chronic Rhinosinusitis.Frontiers in cellular and infection microbiology · 2018Review
- Bitter and sweet taste tests are reflective of disease status in chronic rhinosinusitis.The journal of allergy and clinical immunology. In practiceArticle
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Authors and funding
11 authors.
Funding
Abstract
backgroundSinonasal bitter taste receptors (T2Rs) contribute to upper airway innate immunity and correlate with chronic rhinosinusitis (CRS) clinical outcomes. A subset of T2Rs expressed on sinonasal solitary chemosensory cells (SCCs) are activated by denatonium, resulting in a calcium-mediated secretion of bactericidal antimicrobial peptides (AMPs) in neighboring ciliated epithelial cells. We hypothesized that there is patient variability in the amount of bacterial killing induced by different concentrations of denatonium and that the differences correlate with CRS clinical outcomes.
methodsBacterial growth inhibition was quantified after mixing bacteria with airway surface liquid (ASL) collected from denatonium-stimulated sinonasal air-liquid interface (ALI) cultures. Patient ASL bacterial killing at 0.1 mM denatonium and baseline characteristics and sinus surgery outcomes were compared between these populations.
resultsThere is variability in the degree of denatonium-induced bacterial killing between patients. In CRS with nasal polyps (CRSwNP), patients with increased bacterial killing after stimulation with low levels of denatonium undergo significantly more functional endoscopic sinus surgeries (FESSs) (p = 0.037) and have worse 6-month post-FESS 22-item Sino-Nasal Outcome Test (SNOT-22) scores (p = 0.012).
conclusionBacterial killing after stimulation with low levels of denatonium correlates with number of prior FESS and postoperative SNOT-22 scores in CRSwNP. Some symptoms of CRS in patients with hyperresponsiveness to low levels of denatonium may be due to increased airway immune activity or inherent disease severity.
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