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Am J Rhinol Allergy. 2013 Jul-Aug;27(4):283-6. doi: 10.2500/ajra.2013.27.3911.

The emerging role of the bitter taste receptor T2R38 in upper respiratory infection and chronic rhinosinusitis.

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1
Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA.

Abstract

BACKGROUND:

Maintaining a clean upper respiratory tract requires efficient detection of pathogenic bacteria so that the airway mucosa can mount proper defenses to neutralize and clear the offending microbes. Bitter taste receptors (T2Rs) may play a critical role in this process. T2Rs were originally identified in taste cells of the tongue, where they protect against the ingestion of toxic plant and/or bacterial products. However, T2Rs are also expressed in extragustatory tissue including the airways. One specific T2R isoform, T2R38, was recently shown to be expressed in cilia of sinonasal epithelial cells, suggesting that respiratory cilia may function as a chemosensory organelle, possibly to detect bacterial presence in the airway. T2R38 is encoded by the TAS2R38 gene, which has several common genetic polymorphisms that result in altered receptor functionality. Genetic variation in T2R38 may thus contribute to individual differences in susceptibility to upper airway infection. This study provides an overview of our current knowledge of T2R38 function in sinonasal defense and the implications for patients with chronic rhinosinusitis (CRS).

METHODS:

A literature review was performed of the current knowledge of the bitter taste receptor T2R38 in sinonasal physiology and CRS patient outcomes.

RESULTS:

Basic science research has indicated that the T2R38 receptor is activated by acyl-homoserine lactone (AHL) molecules secreted by gram-negative bacteria, including Pseudomonas aeruginosa. In sinonasal epithelial cells T2R38 stimulates an increase in nitric oxide production that increases mucociliary clearance and directly kills bacteria. Recent clinical studies have also found clinical correlations of TAS2R38 genotype with susceptibility to gram-negative upper respiratory infection as well as necessity for surgical intervention in CRS management.

CONCLUSION:

T2R38 appears to be an important mediator of sinonasal epithelial defense, but further study is needed to more clearly determine how TAS2R38 genotype affects patient outcomes in CRS and other upper airway diseases.

PMID:
23883809
DOI:
10.2500/ajra.2013.27.3911
[Indexed for MEDLINE]
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