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Invasion of human oral epithelial cells by Prevotella intermedia

B R Dorn1, K L Leung, A Progulske-Fox

  • 1Department of Oral Biology, Periodontal Disease Research Center, College of Dentistry, University of Florida, Gainesville, Florida 32608, USA.

Infection and Immunity
|November 24, 1998
PubMed

Insights

Certain Prevotella intermedia bacteria can invade oral epithelial cells, a key factor in periodontal disease. Type C fimbriae and cell rearrangements are essential for this invasion process.

Area of Science:

  • Microbiology
  • Cell Biology
  • Periodontal Disease Research

Background:

  • Pathogenic oral bacteria invasion of epithelial cells is crucial in periodontal disease progression.
  • Prevotella intermedia is a significant oral pathogen implicated in periodontal disease.

Purpose of the Study:

  • To investigate the invasion capabilities of different Prevotella intermedia strains into human oral epithelial cells.
  • To identify bacterial factors and host cell mechanisms involved in P. intermedia invasion.

Main Methods:

  • Utilized a human oral epithelial cell line (KB) and clinical isolates of Prevotella intermedia.
  • Quantified bacterial invasion using antibiotic protection assays and confirmed with electron microscopy.
  • Assessed the role of host cell factors (cytochalasin D, cycloheximide, low temperature) and bacterial components (type C fimbriae antibodies) in invasion.

Main Results:

  • One clinical isolate, P. intermedia strain 17, demonstrated invasion of KB cells, unlike other tested strains.
  • Bacterial internalization was inhibited by cytochalasin D, cycloheximide, monodansylcadaverine, and low temperature, indicating host cell involvement.
  • Antibodies against type C fimbriae and whole P. intermedia cells reduced invasion, with anti-type C fimbriae being more effective.

Conclusions:

  • P. intermedia strain 17 possesses the ability to invade oral epithelial cells.
  • Type C fimbriae and host cell cytoskeletal rearrangements are critical for P. intermedia invasion.
  • This invasion mechanism is a potential virulence factor in periodontal disease pathogenesis.

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