TAS2R16 Activation Suppresses LPS-Induced Cytokine Expression in Human Gingival Fibroblasts

• DOI: 10.3389/fimmu.2021.726546
• Publication Date: 2021-12-15T06:57:41Z
• Authors: Zhiyan Zhou; Ranhui Xi; Jiaxin Liu; Xian Peng; Lei Zhao; Xuedong Zhou; Jiyao Li; Xin Zheng; Xin Xu
• Keywords: Proinflammatory cytokine

Sustained and non-resolved inflammation is a characteristic of periodontitis. Upon acute inflammation, gingival fibroblasts release cytokines to recruit immune cells counter environmental stimuli. The intricate regulation pro-inflammatory signaling pathways, such as NF-κB, necessary maintain periodontal homeostasis. Nonetheless, how resolved has not yet been elucidated. In this study, 22 subtypes taste receptor family 2 (TAS2Rs), well the downstream machineries Gα-gustducin phospholipase C-β2 (PLCβ2), were identified in human (HGFs). Various bitter agonists could induce an intensive cytosolic Ca 2+ response HGFs. More importantly, TAS2R16 was expressed at relatively high level, its agonist, salicin, showed robust evocative effects Activation by salicin inhibited lipopolysaccharide (LPS)-induced cytokines, least part, repressing LPS-induced intracellular cAMP elevation NF-κB p65 nuclear translocation These findings indicate that TAS2Rs activation HGFs may mediate endogenous pro-inflammation resolution antagonizing signaling, providing novel paradigm treatment target for better management