title: Epithelial cell pro-inflammatory cytokine response differs across dental plaque bacterial species.
abstract: OBJECTIVE
  The dental plaque is comprised of numerous bacterial species, which may or may not be pathogenic. Human gingival epithelial cells (HGECs) respond to perturbation by various bacteria of the dental plaque by production of different levels of inflammatory cytokines, which is a putative reflection of their virulence. The aim of the current study was to determine responses in terms of interleukin (IL)-1beta, IL-6, IL-8 and IL-10 secretion induced by Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Streptococcus gordonii in order to gauge their virulence potential.
  
  
  METHODS
  HGECs were challenged with the four bacterial species, live or heat killed, at various multiplicity of infections and the elicited IL-1beta, IL-6, IL-8 and IL-10 responses were assayed by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Primary HGECs challenged with live P. gingivalis produced high levels of IL-1beta, while challenge with live A. actinomycetemcomitans gave high levels of IL-8. The opportunistic pathogen F. nucleatum induces the highest levels of pro-inflammatory cytokines, while the commensal S. gordonii is the least stimulatory.
  
  
  CONCLUSIONS
  We conclude that various dental plaque biofilm bacteria induce different cytokine response profiles in primary HGECs that may reflect their individual virulence or commensal status.
authors.affiliation: Center for Oral Health and Systemic Disease, University of Louisville School of Dentistry, University of Louisville, Louisville, KY, USA.
authors.forename: Panagiota G
authors.initials: PG
authors.lastname: Stathopoulou
authors.forename: Manjunatha R
authors.initials: MR
authors.lastname: Benakanakere
authors.forename: Johnah C
authors.initials: JC
authors.lastname: Galicia
authors.forename: Denis F
authors.initials: DF
authors.lastname: Kinane
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity; D001419:Bacteria / Q000472:pathogenicity*; D001431:Bacteriological Techniques; D002478:Cells, Cultured; D015169:Colony Count, Microbial; D003773:Dental Plaque / Q000382:microbiology*; D004847:Epithelial Cells / Q000382:microbiology; D016967:Fusobacterium nucleatum / Q000472:pathogenicity; D005881:Gingiva / Q000166:cytology / Q000382:microbiology*; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007378:Interleukins / Q000032:analysis*; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D054773:Streptococcus gordonii / Q000472:pathogenicity; D014774:Virulence
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D007378:Interleukins; D016753:Interleukin-10