Does the bitter taste receptor T2R38, expressed on the apical surface of the sinonasal epithelium, serve a sentinel role in microbial quorum-sensing communications and regulate localized innate biocidal defenses against bacterial biofilms associated with chronic rhinosinusitis (CRS)?
Bottom line: When stimulated by AHLs, T2R38 elicits calcium-dependent NO production that increases ciliary beat frequency and mucus clearance. This NO diffuses into the airway and contributes to innate antimicrobial effects.
Explore this issue:January 2017
Background: Multiple investigations have demonstrated an association between sinonasal bacterial biofilms and recalcitrant CRS. The sinonasal cavity is at the front line of defense of the respiratory tract via mucociliary clearance through ciliary beating. When sinonasal ciliated epithelial cells were stimulated with known T2R38-specific agonists, they exhibited calcium-dependent activation of nitric oxide (NO) synthase (NOS).
Study design: Live-cell imaging of DAF-FM in human sinonasal air–liquid interface (ALI) cultures.