Genetic and antigenic analyses of Porphyromonas gingivalis FimA fimbriae

K Nagano1, Y Abiko, Y Yoshida

  • 1Department of Microbiology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan. nagano@dpc.agu.ac.jp

Insights

Porphyromonas gingivalis fimbriae (FimA) show genetic and antigenic diversity across genotypes. FimA expression levels correlate with biofilm formation, and some strains may produce other fimbriae.

Area of Science:

  • Microbiology
  • Oral Health
  • Bacterial Pathogenesis

Background:

  • Porphyromonas gingivalis is a key periodontal pathogen.
  • Fimbriae (FimA and Mfa1) are crucial for biofilm formation.
  • The fimA gene exhibits genetic polymorphism, with six identified genotypes (types I-V and Ib).

Purpose of the Study:

  • To analyze fimA DNA sequences of 84 P. gingivalis strains.
  • To characterize the antigenicity of FimA fimbriae across different genotypes.
  • To investigate the correlation between fimbrial expression, antigenicity, and biofilm formation.

Main Methods:

  • DNA sequencing of the fimA gene from 84 P. gingivalis strains.
  • Antigenicity testing using antisera against purified FimA fimbriae (types I-V).
  • Quantification of fimbrial expression and assessment of biofilm formation on saliva-coated plates.

Main Results:

  • Type Ib fimA sequences were not a single cluster; type II sequences showed high diversity.
  • FimA antigenicity generally correlated with genotype, with cross-reactivity observed (e.g., type Ib with type I, type II with type III).
  • Fimbrial expression levels varied significantly and positively correlated with biofilm formation ability.

Conclusions:

  • P. gingivalis FimA fimbriae display significant genetic and antigenic heterogeneity.
  • Antigenic variation may impact immune recognition and host-pathogen interactions.
  • Fimbrial expression is a key factor in P. gingivalis biofilm formation, a critical aspect of periodontitis pathogenesis.
  • Some P. gingivalis strains may express alternative fimbrial structures beyond FimA and Mfa1.