418 Commensal C. acnes promote epidermal keratinocyte lipid synthesis via PPAR

We observed in human and mouse skin that exposure to C. acnes resulted greatly increased epidermal lipids as indicated by bodily staining hypothesized this microbe may regulate keratinocyte lipid metabolism. To test this, keratinocytes (NHEKs) were exposed sterile supernatant showed a dose dependent increase Oil Red O (p-value <0.001), increases of ceramides, cholesterol free fatty acids detected differential mobility spectrometry-based shotgun lipidomic analysis. Triglycerides the greatest degree; specially those which contain following acids: (16:0), (16:1), (18:1) (18:2). Whole epidermis similar response. Transcriptional analysis further defined pathway for these induced RNA-seq subsequent validation qPCR promoted upregulation genes involved ceramide, acid triglyceride This induction was part short chain (SCFAs) made during its growth (propionic isovaleric acid) SCFAs also accumulation transcription synthesis genes. Activation mediated peroxisome proliferator-activated receptors (PPARs) since siRNA silencing PPARa g NHEKs blocked total or (AGPAT4, GPAT3 DGAT1) when supernatant. effect did not occur upon PPARb. Induction delayed growth. Taken together, results suggest metabolites from trigger decrease survival while influencing barrier host defense.