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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Variations of Porphyromonas gingivalis fimbriae in relation to microbial pathogenesis
Atsuo Amano1, Ichiro Nakagawa, Nobuo Okahashi
1Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan. amanoa@dent.osaka-u.ac.jp
Objectives:
Periodontal disease is an infectious disorder caused by a small subset of periodontal pathogens including Porphyromonas gingivalis. Accumulated evidences show that the expression of P. gingivalis heterogenic virulence properties is dependent on its clonal diversity. P. gingivalis expresses two distinct fimbria molecules, major and minor fimbriae, on its cell surfaces, both of which seem to be involved in the development of periodontitis. In this short review, variations of fimbriae in relation to microbial pathogenesis are discussed.
Materials And Methods:
Our recent findings are summarized to elucidate the relationship between clonal variation of fimbriae and bacterial pathogenicity of various strains.
Results:
Major fimbriae were classified into six types (I to V and Ib) based on the diversity of fimA genes encoding FimA (a subunit of major fimbriae). A majority of periodontitis patients were found to carry type II fimA organisms, followed by type IV, and type II fimA organisms were significantly occurred with more severe forms of periodontitis. Studies of clones with type II fimA have revealed significantly greater adhesive and invasive capabilities to epithelial cells than other fimA type clones. Minor fimbriae induced interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) cytokine expression in macrophages and were suggested to be a causative factor of alveolar bone resorption in animal models. The clonal diversity of minor fimbriae is unclear, however, distinct minor fimbria molecules were found in different strains.
Conclusion:
The fimbria variations may have an influence on the development of periodontal disease.
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