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Porphyromonas gingivalis induces ultrastructural and cytoskeletal changes in adherent human polymorphonuclear

M A Scragg1, M J Kelly, D M Williams

  • 1Department of Oral Pathology, St. Bartholomew's and the Royal London School of Medicine and Dentistry, UK. m.a.scragg@mds.qmw.ac.uk

Journal of Submicroscopic Cytology and Pathology
|November 21, 2000
PubMed

Insights

Porphyromonas gingivalis supernatant suppresses polymorphonuclear leucocyte (PMN) motility. This bacterial mechanism, observed via microscopy, involves PMN shape changes and reduced granule density, contributing to periodontal disease pathogenesis.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Periodontal disease is linked to the bacterium Porphyromonas gingivalis.
  • Polymorphonuclear leucocytes (PMNs) are crucial immune cells in combating oral pathogens.

Purpose of the Study:

  • To investigate the effects of P. gingivalis culture supernatant on human PMN morphology and function.
  • To elucidate potential mechanisms by which P. gingivalis may evade the host immune response.

Main Methods:

  • Human PMNs were exposed to P. gingivalis culture supernatant.
  • Light, fluorescence, and electron microscopy were employed to assess PMN morphology and cytoskeletal changes.
  • Granule density and F-actin levels were quantified.

Main Results:

  • Bacterial supernatant induced a 4-fold increase in spread, flattened PMNs with dendritic projections.
  • Significant reductions in PMN granule density (57%) and F-actin levels (62%) were observed.
  • No loss of PMN viability was detected, indicating suppressed motility rather than cell death.

Conclusions:

  • P. gingivalis supernatant actively suppresses PMN motility through morphological alterations and reduced cytoskeletal components.
  • This suppression mechanism likely contributes to the pathogenic potential of P. gingivalis in periodontal disease.
  • The findings highlight a novel bacterial strategy for immune evasion in the oral cavity.

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