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Titolo:
CONSTRUCTION AND CHARACTERIZATION OF A FIMA MUTANT OF PORPHYROMONAS-GINGIVALIS
Autore:
HAMADA N; WATANABE K; SASAKAWA C; YOSHIKAWA M; YOSHIMURA F; UMEMOTO T;
Indirizzi:
KANAGAWA DENT COLL,DEPT ORAL MICROBIOL,82 INAOKA CHO YOKOSUKA KANAGAWA 238 JAPAN KANAGAWA DENT COLL,DEPT ORAL MICROBIOL YOKOSUKA KANAGAWA 238 JAPAN UNIV TOKYO,INST MED SCI,DEPT BACTERIOL,MINATO KU TOKYO 108 JAPAN AICHI GAKUIN UNIV,SCH DENT,DEPT MICROBIOL,CHIKUSA KU NAGOYA AICHI 464JAPAN
Titolo Testata:
Infection and immunity
fascicolo: 5, volume: 62, anno: 1994,
pagine: 1696 - 1704
SICI:
0019-9567(1994)62:5<1696:CACOAF>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLACK-PIGMENTED BACTEROIDES; HUMAN EPITHELIAL-CELLS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; SURFACE HYDROPHOBICITY; PERIODONTAL-DISEASE; ESCHERICHIA-COLI; ORAL BACTERIA; ADHERENCE; FIMBRIAE; ASACCHAROLYTICUS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
N. Hamada et al., "CONSTRUCTION AND CHARACTERIZATION OF A FIMA MUTANT OF PORPHYROMONAS-GINGIVALIS", Infection and immunity, 62(5), 1994, pp. 1696-1704

Abstract

Although fimbriae of Porphyromonas gingivalis have been implicated asplaying a major role in adherence to gingival tissue surfaces, no conclusive genetic evidence has get been obtained. The fimA gene, the determinant for the major fimbrial subunit protein, was cloned and sequenced (D.P. Dickinson, M.A. Kubiniec, F. Yoshimura, and R.J. Genco, J. Bacteriol. 170:1658-1665, 1988). We undertook to inactivate the fimA gene by a homologous recombination technique and examined the fimA mutant for changes in surface properties, including production of fimbriae,adherence to human gingival fibroblasts and epithelial cells, hemagglutinating activity, and surface hydrophobicity. To inactivate the fimAgene, we disrupted a fimA clone by insertion of a DNA segment containing an erythromycin resistance (Em(r)) gene. This was then delivered into P. gingivalis ATCC 33277 from an Escherichia coli K-12 strain, SM10 lambda pir, by using a mobilizable suicide vector, pGP704; recombination at the fimA locus led to the isolation of a fimA mutant. Disruption of the fimA locus and disappearance of FimA production were confirmed by Southern hybridization with a fimA-specific DNA probe and Western immunoblotting with a monoclonal antibody against the FimA protein, respectively. The fimA mutant constructed failed to express long (0.5-to 1.0-mu m) fimbriae from the bacterial surface and had a diminishedadhesive capacity to tissue-cultured human gingival fibroblasts and epithelial cells. Observation of the bacteria adhering to human gingival fibroblasts by scanning electron microscopy revealed that the wild-type strain had dramatic local changes in the appearance of the microvilli at the point of contact with large bacterial clumps, whereas the fimA mutant did not. In contrast, neither the hemagglutinating activitynor the surface hydrophobicity was changed in the fimA mutant. These data thus constitute the first direct genetic evidence demonstrating that the FimA protein of P. gingivalis is essential for the interactionof the organism with human gingival tissue cells through a function(s) encoded by the fimA gene.

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Documento generato il 27/11/20 alle ore 16:12:18