Primary human sinonasal air-liquid interface cultures were used to elucidate cellular pathways responsive to quorum-sensing molecules, whereas clinical studies investigated the contribution of T2R38 polymorphisms to recalcitrant chronic rhinosinusitis.
Genetic variation in T2R38 functionality has been shown to be associated with susceptibility to upper respiratory tract infections and chronic rhinosinusitis (CRS).
To perform analysis of evidence in current literature on the topic of genetics and chronic rhinosinusitis (CRS), with a particular focus on recent findings in the cystic fibrosis transmembrane regulator (CFTR), genes associated with primary ciliary dyskinesia, and taste receptor T2R38.
The bitter taste receptor T2R38 has been shown to play a role in the pathogenesis of chronic rhinosinusitis (CRS), where the receptor functions to enhance upper respiratory innate immunity through a triad of beneficial immune responses.
Further studies are needed to more clearly determine how TAS2R38 genotype affects patient outcomes in chronic rhinosinusitis and other upper airway diseases.
Recent evidence implicates polymorphisms of the bitter taste receptor TAS2R38 as defining characteristics in respiratory innate defense that may contribute to the complex genetic and environmental interactions predisposing to chronic rhinosinusitis (CRS).
Our objective was to determine whether the nonprotective TAS2R38 polymorphisms, which render the receptor inactive, correlate with medically recalcitrant chronic rhinosinusitis (CRS) necessitating surgical intervention in the context of known risk factors, and thus identify whether the TAS2R38 genotype is an independent risk factor for patients undergoing functional endoscopic sinus surgery (FESS).
This study provides an overview of our current knowledge of T2R38 function in sinonasal defense and the implications for patients with chronic rhinosinusitis (CRS).