Bitter taste receptor T2R14 and autophagy flux in gingival epithelial cells

Abstract

AbstractMacroautophagy (hereafterautophagy) is a lysosomal degradation pathway that functions in nutrient recycling and as a mechanism of innate immunity. Previously we reported, a novel host-bacteria interaction between cariogenicS. mutansand bitter taste receptor (T2R14) in gingival epithelial cells (GEC) leading to an innate immune response. Further,S. mutansmight be using the host immune system to inhibit other Gram-positive bacteria, such asS. aureus. To determine whether these bacteria exploit the autophagic machinery of GEC, it is first necessary to evaluate the role of T2R14 in modulating autophagic flux. So far, the the role of T2R14 in the regulation of autophagy is not well charcterized. Therefore, in this study, for the first time, we report that T2R14 downregulates autophagy flux in GECs and T2R14 knockout increases acidic vacuoles. Transmission electron microscopy morphometric results also suggested increased number of autophagic vesicles in T2R14 knockout GEC. Further, our results suggest thatS. mutanscompetence stimulating peptide CSP-1 showed robust intracellular calcium release and this effect is both T2R14 and autophagy protein 7 dependent. In this study we provide the first evidence that T2R14 modulates autophagy flux in GEC. The results of current study culd have benefitial impact on the identifying the impact of T2R in regulation of immuno microenviroment of GEC and its impact in oral health.