title: Heterogenic virulence and related factors among clinical isolates of Porphyromonas gingivalis with type II fimbriae.
abstract: OBJECTIVE
  Porphyromonas gingivalis is a periodontal pathogen whose fimbriae are classified into six genotypes (types I-V and Ib) based on the diversity of the fimA genes encoding the fimbrial subunits. Accumulated evidence suggests that P. gingivalis strains with type II fimbriae are more virulent as compared to those with other types. However, it is unknown if strong virulence is uniformly conserved among clones with type II fimbriae. In the present study, we compared infectious inflammatory changes in clinical isolates of P. gingivalis with type II fimbriae using a mouse abscess model to examine their pathogenic heterogeneity and heterogeneity-related factors.
  
  
  METHODS
  Suspensions of nine different clinical isolates with type II fimbriae were subcutaneously injected into female BALB/c mice and inflammatory parameters, such as serum sialic acid concentration, were compared.
  
  
  RESULTS
  Many of the type II fimbrial isolates caused severe inflammation in the mice, though some were less causative, as was the control strain ATCC 33277 (type I fimbria strain). These results showed that pathogenic heterogeneity exists among P. gingivalis clones with type II fimbriae. Further, the heterogeneity-related factors of P. gingivalis strains were analyzed and the pathogenic potentials showed positive relationships to gingipain activities and invasive efficiency but not to hydrophobicity or autoaggregation. In addition, invasive efficiency was related to the activities of gingipains that were extracellularly secreted.
  
  
  CONCLUSIONS
  These results suggest that pathogenic heterogeneity has relationships with the invasive and proteolytic activities of P. gingivalis clones with type II fimbriae.
authors.affiliation: Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Inaba
authors.forename: K
authors.initials: K
authors.lastname: Nakano
authors.forename: T
authors.initials: T
authors.lastname: Kato
authors.forename: R
authors.initials: R
authors.lastname: Nomura
authors.forename: S
authors.initials: S
authors.lastname: Kawai
authors.forename: M
authors.initials: M
authors.lastname: Kuboniwa
authors.forename: K
authors.initials: K
authors.lastname: Ishihara
authors.forename: T
authors.initials: T
authors.lastname: Ooshima
authors.forename: A
authors.initials: A
authors.lastname: Amano
mesh_terms: D000038:Abscess / Q000382:microbiology; D018829:Adhesins, Bacterial / Q000032:analysis; D000818:Animals; D001422:Bacterial Adhesion / Q000502:physiology; D016667:Bacterial Capsules / Q000032:analysis; D016866:Bacteroidaceae Infections / Q000382:microbiology; D002478:Cells, Cultured; D003546:Cysteine Endopeptidases / Q000032:analysis; D004195:Disease Models, Animal; D005260:Female; D036781:Fimbriae Proteins / Q000235:genetics; D010861:Fimbriae, Bacterial / Q000145:classification* / Q000235:genetics; D018740:Genetic Heterogeneity; D005838:Genotype; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins / Q000032:analysis; D006801:Humans; D057927:Hydrophobic and Hydrophilic Interactions; D051379:Mice; D008807:Mice, Inbred BALB C; D019158:N-Acetylneuraminic Acid / Q000097:blood; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000472:pathogenicity*; D011897:Random Allocation; D017192:Skin Diseases, Bacterial / Q000382:microbiology; D014774:Virulence / Q000235:genetics / Q000502:physiology*
chemical_list: D018829:Adhesins, Bacterial; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins; C063055:fimbrillin; D036781:Fimbriae Proteins; D003546:Cysteine Endopeptidases; D019158:N-Acetylneuraminic Acid