Inactivation of the Porphyromonas gingivalis fimA gene blocks periodontal damage in gnotobiotic rats

Fimbrial production by Porphyromonas gingivalis was inactivated by insertion-duplication mutagenesis, using the cloned gene for the P. gingivalis major fimbrial subunit protein, fimA. by several criteria, this insertion mutation rendered P. gingivalis unable to produce fimbrilin or an intact fimbria...

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Published in:Journal of bacteriology Vol. 176; no. 4; p. 1052
Main Authors: Malek, R, Fisher, J G, Caleca, A, Stinson, M, van Oss, C J, Lee, J Y, Cho, M I, Genco, R J, Evans, R T, Dyer, D W
Format: Journal Article
Language:English
Published: United States 01.02.1994
Subjects:
Alveolar Bone Loss - microbiology
Animals
Bacterial Adhesion - physiology
Bacterial Proteins - biosynthesis
Bacterial Proteins - genetics
Blotting, Western
Conjugation, Genetic
Durapatite - metabolism
Fimbriae Proteins
Genes, Bacterial - genetics
Germ-Free Life
Hemagglutination Tests
Male
Mutagenesis, Insertional
Mutation
Plasmids - genetics
Porphyromonas gingivalis - genetics
Porphyromonas gingivalis - pathogenicity
Porphyromonas gingivalis - ultrastructure
Rats
Rats, Sprague-Dawley
Recombination, Genetic
Repetitive Sequences, Nucleic Acid
Saliva - metabolism
Streptococcus
Virulence
ISSN:0021-9193
Online Access:Get more information
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Summary:Fimbrial production by Porphyromonas gingivalis was inactivated by insertion-duplication mutagenesis, using the cloned gene for the P. gingivalis major fimbrial subunit protein, fimA. by several criteria, this insertion mutation rendered P. gingivalis unable to produce fimbrilin or an intact fimbrial structure. A nonfimbriated mutant, DPG3, hemagglutinated sheep erythrocytes normally and was unimpaired in the ability to coaggregate with Streptococcus gordonii G9B. The cell surface hydrophobicity of DPG3 was also unaffected by the loss of fimbriae. However, DPG3 was significantly less able to bind to saliva-coated hydroxyapatite than wild-type P. gingivalis 381. This suggested that P. gingivalis fimbriae are important for adherence of the organism to saliva-coated oral surfaces. Further, DPG3 was significantly less able to cause periodontal bone loss in a gnotobiotic rat model of periodontal disease. These observations are consistent with other data suggesting that P. gingivalis fimbriae play an important role in the pathogenesis of human periodontal disease.
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ISSN:0021-9193
DOI:10.1128/jb.176.4.1052-1059.1994