title: Interaction of oral bacteria with gingival epithelial cell multilayers.
abstract: Primary gingival epithelial cells were cultured in multilayers as a model for the study of interactions with oral bacteria associated with health and periodontal disease. Multilayers maintained at an air-liquid interface in low-calcium medium displayed differentiation and cytokeratin properties characteristic of junctional epithelium. Multilayers were infected with fluorescently labeled Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum or Streptococcus gordonii, and bacterial association was determined by confocal microscopy and quantitative image analysis. Porphyromonas gingivalis invaded intracellularly and spread from cell to cell; A. actinomycetemcomitans and F. nucleatum remained extracellular and showed intercellular movement through the multilayer; whereas S. gordonii remained extracellular and predominantly associated with the superficial cell layer. None of the bacterial species disrupted barrier function as measured by transepithelial electrical resistance. P. gingivalis did not elicit secretion of proinflammatory cytokines. However, A. actinomycetemcomitans and S. gordonii induced interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6 and IL-8 secretion; and F. nucleatum stimulated production of IL-1β and TNF-α. Aggregatibacter actinomycetemcomitans, F. nucleatum and S. gordonii, but not P. gingivalis, increased levels of apoptosis after 24 h infection. The results indicate that the organisms with pathogenic potential were able to traverse the epithelium, whereas the commensal bacteria did not. In addition, distinct host responses characterized the interaction between the junctional epithelium and oral bacteria.
authors.affiliation: Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA.
authors.forename: B C
authors.initials: BC
authors.lastname: Dickinson
authors.forename: C E
authors.initials: CE
authors.lastname: Moffatt
authors.forename: D
authors.initials: D
authors.lastname: Hagerty
authors.forename: S E
authors.initials: SE
authors.lastname: Whitmore
authors.forename: T A
authors.initials: TA
authors.lastname: Brown
authors.forename: D T
authors.initials: DT
authors.lastname: Graves
authors.forename: R J
authors.initials: RJ
authors.lastname: Lamont
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology / Q000502:physiology; D017209:Apoptosis / Q000502:physiology; D001419:Bacteria / Q000276:immunology / Q000472:pathogenicity*; D018929:Cell Culture Techniques; D004846:Epithelial Attachment / Q000166:cytology / Q000276:immunology / Q000382:microbiology*; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D016967:Fusobacterium nucleatum / Q000276:immunology / Q000502:physiology; D005881:Gingiva / Q000166:cytology / Q000276:immunology / Q000382:microbiology*; D054884:Host-Pathogen Interactions; D006801:Humans; D007091:Image Processing, Computer-Assisted; D018836:Inflammation Mediators / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D053535:Keratin-13 / Q000032:analysis; D053534:Keratin-9 / Q000032:analysis; D018613:Microscopy, Confocal; D009061:Mouth Mucosa / Q000382:microbiology*; D010510:Periodontal Diseases / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology / Q000502:physiology; D054773:Streptococcus gordonii / Q000276:immunology / Q000502:physiology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D053535:Keratin-13; D053534:Keratin-9; D014409:Tumor Necrosis Factor-alpha