title: Effect of growth factors on antimicrobial peptides and pro-inflammatory mediators during wound healing.
abstract: BACKGROUND
  Antimicrobial peptides (AMPs), such as human beta-defensin-2 (hBD-2) and the CC-chemokine ligand 20 (CCL20), exhibit direct microbicidal effects and mediator-like activity. It was hypothesized that wounding induces the expression of AMPs and pro-inflammatory mediators and that endogenous mediators, such as insulin-like growth factor-1 (IGF-1) and transforming growth factor-alpha (TGF-alpha), modulate this induced expression.
  
  
  METHODS
  Monolayers of gingival epithelial cells (GECs) and gingival fibroblast (HGFs) from three different donors were wounded using the scratch assay (in vitro wounding) in the presence (test group) or absence (control group) of IGF-1 and TGF-alpha. In vitro wound closure was monitored over time (0, 6, 24, 48, 72 h), and wound areas were microscopically analyzed (Axio-Vision® Software, Zeiss). Gene expression analysis of the GAPDH, hBD-2, CCL20, interleukin-1 beta (IL-1 beta), and interleukin-8 (IL-8) was performed by qPCR.
  
  
  RESULTS
  In comparison to control cells, IGF-1 and TGF-alpha significantly enhanced in vitro wound closure (P < 0.05). In GECs, IGF-1 induced the gene expression of IL-1 beta and IL-8 when compared to control cells (P < 0.05). In HGFs, wounding per se induced the messenger RNA of hBD-2, CCL20, and IL-1 beta, whereas IGF-1 and TGF-alpha reversed this effect (P < 0.05).
  
  
  CONCLUSIONS
  In gingival cells, the gene expression of AMPs was altered by injury, and endogenous growth factors further influenced the expression profiles, but with high interindividual differences.
authors.affiliation: Department of Periodontology, Operative and Preventive Dentistry, University Hospital Bonn, Welschnonnenstraße 17, 53111, Bonn, Germany, dommisch@uni-bonn.de.
authors.forename: H
authors.initials: H
authors.lastname: Dommisch
authors.forename: J
authors.initials: J
authors.lastname: Winter
authors.forename: W
authors.initials: W
authors.lastname: Götz
authors.forename: J
authors.initials: J
authors.lastname: Miesen
authors.forename: A
authors.initials: A
authors.lastname: Klein
authors.forename: L
authors.initials: L
authors.lastname: Hierse
authors.forename: J
authors.initials: J
authors.lastname: Deschner
authors.forename: A
authors.initials: A
authors.lastname: Jäger
authors.forename: J
authors.initials: J
authors.lastname: Eberhard
authors.forename: S
authors.initials: S
authors.lastname: Jepsen
mesh_terms: D000890:Anti-Infective Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D010455:Peptides / Q000494:pharmacology*; D014945:Wound Healing
chemical_list: D000890:Anti-Infective Agents; D018836:Inflammation Mediators; D010455:Peptides