Abstract
Taste receptors, first identified on the tongue, are best known for their role in guiding our dietary preferences. The expression of taste receptors for umami, sweet, and bitter have been demonstrated in tissues outside of the oral cavity, including in the airway, brain, gastrointestinal tract, and reproductive organs. The extra-oral taste receptor chemosensory pathways and the endogenous taste receptor ligands are generally unknown, but there is increasing data suggesting that taste receptors are involved in regulating some aspects of innate immunity, and may potentially control the composition of the nasal microbiome in healthy individuals or patients with upper respiratory diseases like chronic rhinosinusitis (CRS). For this reason, taste receptors may serve as potential therapeutic targets, providing alternatives to conventional antibiotics. This review focuses on the physiology of sweet (T1R) and bitter (T2R) taste receptors in the airway and their activation by secreted bacterial products. There is particular focus on T2R38 in sinonasal ciliated cells, as well as the sweet and bitter receptors found on specialized sinonasal solitary chemosensory cells. Additionally, this review explores the impact of genetic variations in these receptors on the differential susceptibility of patients to upper airway infections, such as CRS.
Highlights
The sinonasal cavity, which includes the nose and four paired sinuses, serves as the forward line of immune defense against inhaled pathogens [1,2]
Recent research has demonstrated an association between sinonasal innate immunity and sweet and bitter taste receptors, suggesting that taste receptors could be pharmacologically targeted to treat the pathophysiology of chronic rhinosinusitis (CRS) and/or other types of respiratory infections
This review found that airway cilia T2Rs are potential receptors for two quinolone quorum sensing molecules produced by P. aeruginosa [84,85]
Summary
The sinonasal cavity, which includes the nose and four paired sinuses, serves as the forward line of immune defense against inhaled pathogens [1,2]. The sinonasal epithelial lining utilizes a process termed mucociliary clearance (MCC) as its primary physical defense mechanism to trap and clear inhaled debris and microbes. This unique mechanism is part of the innate immune system and is dependent on mucus secretion and effective ciliary beating. When the sinonasal immune defense is impaired, individuals can develop diseases, such as chronic rhinosinusitis (CRS), a multifaceted disease frequently characterized by stasis of secretions from impaired MCC and persistent inflammation and infection in the upper airway [3,5,6]. The trapped pathogens are eliminated from the airway through mucociliary clearance (MCC), most important physical defense against these inhaled irritants and microbes.
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