1355 TRPV3 mediates cutibacterium acnes-induced chemotaxis and inflammation in sebocytes

TRPV3 mediates itch and inflammation in keratinocytes plays an important role atopic dermatitis, however, whether how is involved the pathogenesis of acne remains unclear. Thus, we explored effects on sebaceous glands (SGs) inflammation, its relation to cutibacterium acnes (C.acnes), underlying mechanisms vitro vivo. Our study found that overexpression activated Toll-like receptor 2 (TLR2)- Nuclear factor kappa-B (NF-κB) signal pathway promoted release acne-related inflammatory cytokines chemokines significantly (ranged from 1 7 fold, p＜0.05), which contributed chemotaxis neutrophils SZ95 sebocytes further amplified responses. Conversely, genetic deletion or pharmacological inhibition by specific inhibitor both ameliorated phenotype human C.acnes-induced acne-like mouse model. Mechanistically, C.acnes could upregulate expression TRPV3, activates NF-κB signaling regulating TLR2 subsequently promote downstream releases. In conclusion, our revealed a previously unreported association between C.acnes, development may suggest as novel therapeutic target for vulgaris other disorders pilosebaceous unit.