Additional Supporting Information may be found in the online version of this article.
Solitary chemosensory cells and bitter taste receptor signaling in human sinonasal mucosa
Article first published online: 12 FEB 2013
© 2013 ARS-AAOA, LLC
International Forum of Allergy & Rhinology
Volume 3, Issue 6, pages 450–457, June 2013
How to Cite
How to Cite this Article: Solitary chemosensory cells and bitter taste receptor signaling in human sinonasal mucosa. Int Forum Allergy Rhinol, 2013; 3:450–457., , , et al.
Funding sources for the study: American Academy of Otolaryngology, ARS Resident Research Grant #235218 to HPB; NIH grants R01DC009820 through NIDCD to TEF and SCK, and P30DC004657 to Diego Restrepo PhD.
Potential conflict of interest: V.R.R. is a research consultant for Arthrocare.
- Issue published online: 25 JUN 2013
- Article first published online: 12 FEB 2013
- Manuscript Accepted: 7 DEC 2012
- Manuscript Revised: 29 NOV 2012
- Manuscript Received: 17 AUG 2012
- American Academy of Otolaryngology. Grant Number: #235218
- NIH. Grant Number: R01DC009820
- TEF and SCK. Grant Number: P30DC004657
- bitter taste transduction;
- respiratory epithelium;
- solitary chemosensory cell
Solitary chemosensory cells (SCCs) are specialized cells in the respiratory epithelium that respond to noxious chemicals including bacterial signaling molecules. SCCs express components of bitter taste transduction including the taste receptor type 2 (TAS2R) bitter taste receptors and downstream signaling effectors: α-Gustducin, phospholipase Cβ2 (PLCβ2), and transient receptor potential cation channel subfamily M member 5 (TRPM5). When activated, SCCs evoke neurogenic reflexes, resulting in local inflammation. The purpose of this study was to test for the presence SCCs in human sinonasal epithelium, and to test for a correlation with inflammatory disease processes such as allergic rhinitis and chronic rhinosinusitis.
Patient demographics and biopsies of human sinonasal mucosa were obtained from control patients (n = 7) and those with allergic rhinitis and/or chronic rhinosinusitis (n = 15). Reverse transcription polymerase chain reaction (RT-PCR), quantitative PCR (qPCR), and immunohistochemistry were used to determine whether expression of signaling effectors was altered in diseased patients.
RT-PCR demonstrated that bitter taste receptors TAS2R4, TAS2R14, and TAS2R46, and downstream signaling effectors α-Gustducin, PLCβ2, and TRPM5 are expressed in the inferior turbinate, middle turbinate, septum, and uncinate of both control and diseased patients. PLCβ2/TRPM5-immunoreactive SCCs were identified in the sinonasal mucosa of both control and diseased patients. qPCR showed similar expression of α-Gustducin and TRPM5 in the uncinate process of control and diseased groups, and there was no correlation between level of expression and 22-item Sino-Nasal Outcomes Test (SNOT-22) or pain scores.
SCCs are present in human sinonasal mucosa in functionally relevant areas. Expression level of signaling effectors was similar in control and diseased patients and did not correlate with measures of pain and inflammation. Further study into these pathways may provide insight into nasal inflammatory diseases and may offer potential therapeutic targets.