title: Expression of CD1a monocytes cultured with supernatants from periodontally diseased gingival epithelial cells.
abstract: Langerhans cells are believed to originate from the monocyte lineage and have been reported to increase in number with plaque accumulation and gingival inflammation. The aim of this study was to investigate the effects of local gingival epithelial factors on the induction of CD1a, a Langerhans cell phenotype, on monocyte rich populations.
  
  
  METHODS
  Peripheral blood monocyte rich in populations from healthy subjects were cultured for 24 h with either healthy gingival or periodontally diseased gingival epithelial supernatants. Additionally, the monocyte rich populations were cultured with cytokines IL-I alpha, IL-I beta, IL-6 and TNF-alpha which are known to be produced by epithelial cells or co-cultured with autologous epithelial cells. The per cent CD1a positive cells was determined using FACS analysis.
  
  
  RESULTS
  Healthy gingival supernatants did not induce CD1a expression in monocyte rich populations, however, a significant increase in per cent CD1a+ cells for monocyte rich populations cultured with five (P < 0.01) of six periodontal gingival epithelial supernatants was found. IL-I alpha or TNF-alpha (10 ng/well) resulted in a significant increase in the per cent CD1a+ cells (P < 0.01). Depletion of CD1a+ Langerhans cells from healthy gingival epithelium did not enhance induction of CD1a expression in monocyte rich populations. Monocyte rich populations cultured together with non-depleted epithelial cultures resulted in a decreased per cent of CD1a+ cells.
  
  
  CONCLUSIONS
  These findings indicated that epithelial factor/s associated with periodontally involved epithelia, may be involved in inducing a Langerhans cell phenotype in monocyte rich populations. The data also provide indirect evidence for a role of Langerhans cells in inhibiting induction of CD1a in healthy epithelium.
authors.affiliation: Department of Dentistry, University of Adelaide, Australia.
authors.forename: T
authors.initials: T
authors.lastname: Winning
authors.forename: E
authors.initials: E
authors.lastname: Gemmell
authors.forename: B
authors.initials: B
authors.lastname: Polak
authors.forename: N W
authors.initials: NW
authors.lastname: Savage
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
authors.forename: L J
authors.initials: LJ
authors.lastname: Walsh
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D018949:Antigens, CD1 / Q000096:biosynthesis*; D019070:Cell Lineage; D002478:Cells, Cultured; D018920:Coculture Techniques; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology; D005881:Gingiva / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology; D007801:Langerhans Cells / Q000166:cytology* / Q000276:immunology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D010518:Periodontitis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D018949:Antigens, CD1; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha