Abstract：
:Solitary chemosensory cells (SCCs) are epithelial sentinels that utilize bitter Tas2r receptors and coupled taste transduction elements to detect pathogenic bacterial metabolites, triggering host defenses to control the infection. Here we report that SCCs are present in mouse gingival junctional epithelium, where they express several Tas2rs and the taste signaling components α-gustducin (Gnat3), TrpM5, and Plcβ2. Gnat3-/- mice have altered commensal oral microbiota and accelerated naturally occurring alveolar bone loss. In ligature-induced periodontitis, knockout of taste signaling molecules or genetic absence of gingival SCCs (gSCCs) increases the bacterial load, reduces bacterial diversity, and renders the microbiota more pathogenic, leading to greater alveolar bone loss. Topical treatment with bitter denatonium to activate gSCCs upregulates the expression of antimicrobial peptides and ameliorates ligature-induced periodontitis in wild-type but not in Gnat3-/- mice. We conclude that gSCCs may provide a promising target for treating periodontitis by harnessing innate immunity to regulate the oral microbiome.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Zheng X,Tizzano M,Redding K,He J,Peng X,Jiang P,Xu X,Zhou X,Margolskee RFdoi
10.1038/s41467-019-12505-xsubject
Has Abstractpub_date
2019-10-03 00:00:00pages
4496issue
1issn
2041-1723pii
10.1038/s41467-019-12505-xjournal_volume
10pub_type
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