Bitter taste receptors of the taste receptor family 2 (T2R) were initially found and named based on their involvement in type 2 taste cells of the tongue, where they detect the presence of potentially hazardous ingested substances. T2R receptors were discovered in airway epithelial cells in 2009, but their significance in airway physiology and human illness has just recently been discovered. Recent studies have shown that released bacterial products activate at least one airway T2R receptor, taste receptor family 2 isoform 38 protein (T2R38). T2R38 activation in sinonasal epithelial cells increases nitric oxide generation, increases ciliary beating, and directly kills germs. TAS2R38 genotype has also been linked to susceptibility to gram-negative upper respiratory infections in clinical trials, and T2R38 has been identified as an independent risk factor for chronic rhinosinusitis needing sinus surgery.

T2R38 has been implicated in sinonasal innate immunity and chronic rhinosinusitis in recent research. The possible development of T2R38-directed topical treatments, as well as the use of taste testing and/or genotyping to predict susceptibility to infection, have clinical implications. More research is needed to establish how the TAS2R38 genotype impacts patient outcomes in chronic rhinosinusitis and other upper airway disorders.

Reference:https://journals.lww.com/co-allergy/Abstract/2015/02000/Role_of_the_bitter_taste_receptor_T2R38_in_upper.3.aspx