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Updated: Jul 7, 2026

Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

Published on: December 17, 2015

P. gingivalis accelerates gingival epithelial cell progression through the cell cycle.

Masae Kuboniwa¹, Yoshiaki Hasegawa, Song Mao

¹Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Osaka, Japan.

Microbes and Infection

|February 19, 2008

Summary

Periodontal pathogen P. gingivalis accelerates gingival epithelial cell proliferation by altering cell cycle proteins. This effect, crucial for P. gingivalis pathogenesis, depends on its long fimbriae.

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Isolation, Processing and Analysis of Murine Gingival Cells

Isolation, Processing and Analysis of Murine Gingival Cells

Published on: July 2, 2013

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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

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Published on: December 17, 2015

Isolation, Processing and Analysis of Murine Gingival Cells

Isolation, Processing and Analysis of Murine Gingival Cells

Published on: July 2, 2013

Area of Science:

Microbiology
Cell Biology
Periodontal Disease Research

Background:

* *Porphyromonas gingivalis* (P. gingivalis) is an opportunistic pathogen implicated in periodontal disease.
* P. gingivalis resides within gingival epithelial cells, the primary barrier in the gingival crevice.

Purpose of the Study:

* To investigate the impact of P. gingivalis infection on the cell cycle of gingival epithelial cells.
* To identify host cell pathways affected by P. gingivalis and the role of bacterial fimbriae.

Main Methods:

* Proteomic analysis of infected gingival epithelial cells.
* Cytofluorimetry to assess cell proliferation and cell cycle progression.
* Comparison of wild-type P. gingivalis with mutant strains lacking long fimbriae.

Main Results:

* P. gingivalis infection broadly alters protein levels and phosphorylation, affecting cell cycle control.
* Key cell cycle pathways, including cyclins, p53, and PI3K, were impacted.
* Infected cells exhibited enhanced proliferation and accelerated S-phase progression.
* Elevated proliferation was dependent on the presence of P. gingivalis long fimbriae.

Conclusions:

* P. gingivalis infection promotes gingival epithelial cell proliferation.
* This accelerated cell cycling, mediated by bacterial fimbriae, may have significant implications for gingival tissue homeostasis and disease pathogenesis.
* Understanding these mechanisms is vital for developing targeted therapies for periodontal disease.