The bittersweet taste of bacteria in the nose of patients with chronic rhinosinusitis with nasal polyps.

The nasal epithelium forms the first line of defense against environmental insults. Damage to epithelial structure and function, is involved in the pathology of chronic rhinosinusitis with nasal polyps (CRSwNP). Bitter (T2R) and sweet (T1R) taste receptors are upper airway sensors that detect and induce a rapid immune response against secreted bacterial ligands. Activation of T2Rs on nasal epithelium results in rapid calcium release that stimulates the secretion of antimicrobial compounds and production of nitric oxide, consequently killing the bacteria and increasing ciliary beating. Activation of T1R antagonizes the host’s T2R mediated immune response. Moreover, T1R agonists increase bacterial survival and propagation. In line with this, we have previously demonstrated that patients with CRSwNP have an increased presence of pathogenic bacteria and a decrease in beneficial lactic acid bacteria, which are able to modulate barrier homeostasis. Unfortunately, limited studies focus on the relationship between the nasal microbiome and taste receptor function in CRSwNP patients. As such, in this project we will investigate the effect of bacterial ligands, produced by the nasal microbiome, on taste receptor function in CRSwNP.