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Am J Rhinol Allergy. 2014 Sep-Oct;28(5):366-73. doi: 10.2500/ajra.2014.28.4077.

Sinonasal solitary chemosensory cells "taste" the upper respiratory environment to regulate innate immunity.

Author information

1
Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Abstract

BACKGROUND:

It is not fully understood how sinonasal epithelial cells detect the presence of pathogens and activate innate defense responses necessary for protecting the upper airway from infection. One mechanism is through bitter taste receptors (T2Rs), which are expressed in the sinonasal cavity. One T2R isoform, T2R38, is expressed in ciliated cells and detects quorum-sensing molecules from gram-negative bacteria, activating antimicrobial nitric oxide production. More recent studies have examined the role of T2Rs expressed in a sinonasal cell type that has only recently been identified in humans, the solitary chemosensory cell (SCC). We sought to provide an overview of SCCs and taste receptor function in human sinonasal defense as well as implications for chronic rhinosinusitis (CRS).

METHODS:

A literature review of the current knowledge of SCCs and taste receptors in sinonasal physiology and CRS was conducted.

RESULTS:

Human sinonasal SCCs express both bitter T2R and sweet T1R2/3 receptors. Activation of SCC T2Rs activates a calcium signal that propagates to the surrounding epithelial cells and causes secretion of antimicrobial peptides. T1R2/3 sweet receptor activation by physiological airway surface liquid (ASL) glucose concentrations attenuates the T2R response, likely as a mechanism to prevent full activation of the T2R pathway except during times of infection, when pathogens may consume ASL glucose and reduce its concentration.

CONCLUSION:

SCCs appear to be important mediators of upper airway innate immunity, as the SCC T2Rs regulate antimicrobial peptide secretion, but further study is needed to determine the specific T2R isoforms involved as well as whether polymorphisms in these isoforms affect susceptibility to infection or patient outcomes in CRS. The inhibitory role of T1R2/3 sweet receptor suggests that T1R2/3 blockers may have therapeutic potential in some CRS patients, particularly those with diabetes mellitus. However, further clinical study of the relationship between infection and T1R2/3 genotype is required.

PMID:
25198020
DOI:
10.2500/ajra.2014.28.4077
[Indexed for MEDLINE]

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