title: The induction expression of human β-defensins in gingival epithelial cells and fibroblasts.
abstract: OBJECTIVE
  The gingival epithelial cells and fibroblasts can produce antimicrobial peptides when stimulated by inflammatory cytokines. The purpose of the present study was to test whether gingival keratinocytes and gingival fibroblasts respond differently to inflammatory cytokine activation. This will enable us to understand the chronic inflammatory response in the process of periodontal disease.
  
  
  METHODS
  Gingival keratinocytes and fibroblasts were isolated and treated with different concentrations of IL-1β and quantitative real-time PCR was performed to evaluate the induced expressions of hBD-1, hBD-2 and hBD-3. The induced response was compared between the gingival epithelial cells and fibroblasts. The inhibitors of p38 protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) were applied to explore the molecular mechanism during the induction of hBDs in both cells.
  
  
  RESULTS
  The results showed that the hBDs expressions were found to be induced by different concentrations of IL-1β, but with several differences between gingival epithelial cells and fibroblasts. The hBDs mRNA expression in gingival fibroblasts was more sensitive compared with keratinocytes to different concentrations of IL-1β. The hBD-1 and hBD-3 expressions in these two cells were down-regulated by IL-1β and hBD-2 expression was up-regulated. The inflammatory cytokine IL-1β had dual effect on hBDs expression.
  
  
  CONCLUSIONS
  The gingival epithelial cells and fibroblasts respond differently to the inflammatory cytokine IL-1β which indicated different roles played by the two cells in the host defense. The dual effect of IL-1β on hBDs expression may contribute to the defensins down-regulation in periodontal disease.
authors.affiliation: Department of Stomatology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, PR China. Electronic address: kqyyljr@yahoo.com.cn.
authors.forename: Jiarong
authors.initials: J
authors.lastname: Liu
authors.forename: Xingyan
authors.initials: X
authors.lastname: Du
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Hu
authors.forename: Lili
authors.initials: L
authors.lastname: Chen
mesh_terms: D001706:Biopsy; D002478:Cells, Cultured; D005347:Fibroblasts / Q000378:metabolism*; D005881:Gingiva / Q000166:cytology* / Q000378:metabolism*; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology*; D015603:Keratinocytes / Q000378:metabolism*; D016328:NF-kappa B / Q000494:pharmacology; D060888:Real-Time Polymerase Chain Reaction; D013778:Tetrazolium Salts; D013844:Thiazoles; D023083:beta-Defensins / Q000096:biosynthesis*; D048051:p38 Mitogen-Activated Protein Kinases / Q000494:pharmacology
chemical_list: D053583:Interleukin-1beta; D016328:NF-kappa B; D013778:Tetrazolium Salts; D013844:Thiazoles; D023083:beta-Defensins; D048051:p38 Mitogen-Activated Protein Kinases; C022616:thiazolyl blue
keywords: Antimicrobial; Cell response; Innate immune; Periodontal disease