title: CBT-SL5, a bacteriocin from Enterococcus faecalis, suppresses the expression of interleukin-8 induced by Propionibacterium acnes in cultured human keratinocytes.
abstract: Propionibacterium acnes is known to play a pivotal role in the pathogenesis of acne vulgaris. CBT-SL5 is one of the antimicrobial peptides from Enterococcus faecalis SL5, and it has shown antimicrobial activity against P. acnes. The aim of this study was to investigate the anti-inflammatory effect of CBT-SL5 on the inflammation induced by P. acnes in cultured human keratinocyes. Cultured human keratinocytes derived from neonatal foreskin were treated with heatkilled P. acnes to induce inflammation, and then various concentrations of CBT-SL5 were added to the P. acnestreated keratinocytes. The mRNA expression and protein secretion of interleukin (IL)-8, an inflammation marker, was analyzed by real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. We also analyzed the nuclear factor-kappa B (NF-kappaB) p65 translocation by performing immunofluorescent staining. P. acnes treatment upregulated the IL-8 mRNA expression in the keratinocytes, and this was brought about through both toll-like receptor (TLR)2 and TLR4. At the concentrations of 10, 50, and 100 ng/ml, CBT-SL5 significantly downregulated the P. acnes-induced IL-8 mRNA expression and protein production (p<0.05). At 6 h and 12 h of the treatment, CBT-SL5 significantly suppressed the P. acnesinduced IL-8 mRNA expression. Secretion of IL-8 protein was significantly reduced at 24 h. The functional inhibitory activity of CBT-SL5 was shown by CBT-SL5 suppressing the P. acnes-induced NF-kappaB translocation from the cytoplasm to the nucleus. These results demonstrated that CBT-SL5 suppressed the P. acnes-induced IL-8 expression in keratinocytes. Therefore, CBT-SL5 may be a novel anti-inflammatory treatment for acne.
authors.affiliation: Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Ye Jin
authors.initials: YJ
authors.lastname: Lee
authors.forename: Hye Jeong
authors.initials: HJ
authors.lastname: Choi
authors.forename: Tae Wook
authors.initials: TW
authors.lastname: Kang
authors.forename: Hyung Ok
authors.initials: HO
authors.lastname: Kim
authors.forename: Myung Jun
authors.initials: MJ
authors.lastname: Chung
authors.forename: Young Min
authors.initials: YM
authors.lastname: Park
mesh_terms: D000152:Acne Vulgaris / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001430:Bacteriocins / Q000494:pharmacology*; D002478:Cells, Cultured; D015536:Down-Regulation; D013293:Enterococcus faecalis / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects*; D006801:Humans; D016209:Interleukin-8 / Q000235:genetics* / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D011425:Propionibacterium acnes / Q000187:drug effects*; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D001430:Bacteriocins; D016209:Interleukin-8; D016328:NF-kappa B; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4