title: β-defensin 3 modulates macrophage activation and orientation during acute inflammatory response to Porphyromonas gingivalis lipopolysaccharide.
abstract: β-defensin 3, a multifunctional antimicrobial peptide, has immuno-regulatory activities. We investigated the modulatory mechanism of human β-defensin 3 (hBD3) on acute inflammatory response resulted from Porphyromonas gingivalis lipopolysaccharide (P.g-LPS), which plays a pro-inflammatory role in periodontal infection and its derived systemic inflammation. P.g-LPS was administrated to mice and murine macrophages alone or along with hBD3. P.g-LPS could lead to acute inflammation as soon as 2h. And it was observed that hBD3 significantly decreased the production of pro-inflammatory biomarkers of in response to P.g-LPS in vivo and in vitro in the early stage. Interestingly, although hBD3 as well as P.g-LPS stimulated the expression of TLR2 mRNA in macrophages in this study, hBD3 exhibited suppressive effect on the downstream NF-κB signaling pathway activated by P.g-LPS. And above all, hBD3 could polarize macrophages into M2 phenotype and this contributed to its anti-inflammatory property. These results indicated that hBD3 could have therapeutic effect on systemic inflammation associated with periodontal infections via modulating macrophage activation and orientation.
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Jinglu
authors.initials: J
authors.lastname: Lyu
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Tianying
authors.initials: T
authors.lastname: Bian
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Chen
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Di
authors.initials: D
authors.lastname: Cui
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Li
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Gong
authors.affiliation: Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China. Electronic address: yanfh@nju.edu.cn.
authors.forename: Fuhua
authors.initials: F
authors.lastname: Yan
mesh_terms: D000208:Acute Disease; D000818:Animals; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides / Q000737:chemistry / Q000633:toxicity*; D008262:Macrophage Activation / Q000187:drug effects* / Q000235:genetics; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics / Q000276:immunology; D023083:beta-Defensins / Q000494:pharmacology*
chemical_list: C422950:DEFB103A protein, human; D008070:Lipopolysaccharides; D016328:NF-kappa B; D023083:beta-Defensins
keywords: Immuno-regulatory; Macrophage orientation; P.g-LPS; β-defensin 3