Experimental Porphyromonas gingivalis infection in nonimmune athymic BALB/c mice

Chen, P B; Davern, Lynda B.; Aguirre, Alfredo

doi:10.1128/iai.59.12.4706-4709.1991

Cited by 26 publications

(20 citation statements)

References 18 publications

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“…The capsule of P. gingivalis lowers the hydrophobicity of the bacterial surface (Andrian et al, 2006). WT (II) is encapsulated, whereas WT (I) is not (Grenier and Mayrand, 1987;Chen et al, 1991). Bacterial hydrophobicity is thought to promote bacterial interactions with host proteins and readily phagocytosis by leucocytes (Sundqvist et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Virulence of Porphyromonas gingivalis is altered by substitution of fimbria gene with different genotype

Kato¹,

Kawai²,

Nakano

et al. 2007

Cell Microbiol

114

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SummaryPorphyromonas gingivalis is a periodontal pathogen whose fimbriae are classified into six genotypes based on the diversity of the fimA genes encoding each fimbria subunit. It was suggested that P. gingivalis strains with type II fimbriae were more virulent than type I strains. For the present study, we generated the mutants in which fimA was substituted with different genotypes to study virulence of type II fimbriae. Using plasmid vectors, fimA of ATCC33277 (type I strain) was substituted with type II fimA, and that of OMZ314 (type II strain) with type I fimA. The substitution of type I fimA with type II enhanced bacterial adhesion/invasion to epithelial cells, whereas substitution with type I fimA resulted in diminished efficiency. Following bacterial invasion, type II clones swiftly degraded cellular paxillin and focal adhesion kinase, and inhibited cellular migration, whereas type I clones and DfimA mutants did not. BIAcore analysis demonstrated that type II fimbriae possess greater adhesive abilities for their receptor a5b1-integrin than those of type I. In a mouse abscess model, the type II clones significantly induced serum IL-1b and IL-6, as well as other infectious symptoms. These results suggest that type II fimbriae are a critical determinant of P. gingivalis virulence.

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Section: Discussionmentioning

confidence: 99%

Virulence of Porphyromonas gingivalis is altered by substitution of fimbria gene with different genotype

Kato¹,

Kawai²,

Nakano

et al. 2007

Cell Microbiol

114

View full text Add to dashboard Cite

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“…The role of T cells populations in enhanced host pathogenesis or protection from challenge with invasive strain of P. gingivalis has not been defined. In one study involving infection of athymic nude (nu/nu) mice and their heterozygous (nu/-i-) littermates with P. gingivalis, results were presented suggesting that T lymphocytes may enhance the pathogenesis seen in nu/+ mice since the nu/nu mice were able to localize invasive strains of P. gingivalis (8). Since the nu/nu mice did not make anti-P. gingivalis antibodies, the role of specific antibodies to periodontal pathogens in preventing an invasive infection needs further study.…”

Section: Discussionmentioning

confidence: 99%

Host responses induced by co‐infection with Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in a murine model

Chen

Davern

Katz

et al. 1996

Oral Microbiology and Immunology

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In this study, evidence is presented that mixed infection with the periodontal pathogens Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans results in a synergistic effect in their pathogenicity and in their ability to induce humoral and cellular host responses. BALB/c mice were injected subcutaneously on the back with P. gingivalis ATCC 53977, A. actinomycetemocomitans 75 or a mixture of both bacteria. Samples of blood and fluid from abscesses formed at the site of injection (first degree) or distant from the injection site were collected for microbiologic analysis. Serum and spleens were obtained for evaluation of humoral and cellular responses to P. gingivalis and A actinomycetemocomitans. Mice injected with A. actinomycetemcomitans had first-degree lesions only, whereas mice injected with P. gingivalis and A. actinomycetemcomitans had lesions at first- and second-degree sites from which both bacterial species were isolated. A serum anti-P. gingivalis response was induced in P. gingivalis-injected mice, which was higher in mice injected with P. gingivalis and A. actinomycetemcomitans. This pattern was not seen in the anti-A, actinomycetemcomitans response. Lymphoproliferative responses to phytohemagglutinin, Escherichia coli lipopolysaccharide and P. gingivalis of spleen cells from infected mice were decreased, especially following co-infection. Furthermore, co-infection of mice resulted in the greatest decrease in the number of CD5+, especially CD4+ lymphocytes.

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“…Numerous animaJ models have been developed which have been extremely valuable in providing information important to our understanding of virulence properties of P. gingivalis (1,3,4,10,11,13,17,18,21,22). For instance.…”

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confidence: 99%

Effect of host responses on the pathogenicity of strains of Porphyromonas gingivalis

Katz¹,

Ward

Michalek

1996

Oral Microbiology and Immunology

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Porphyromonas gingivalis is implicated in the etiology of periodontitis. Strains of P. gingivalis have been classified as invasive or noninvasive based on their ability to form abscesses in a mouse model. The purpose of this study was to investigate the ability of P. gingivalis strains to cause abscesses and periodontal bone loss in an experimental rat model and the effect of serum and salivary responses on the pathogenicity of these strains. Subcutaneous injection of animals with P. gingivalis 33277, A7A1-28, W50 or 381 resulted in abscesses in a higher percentage of mice than rats. P. gingivalis 33277 caused lesions at the site of injection, whereas strains A7A1-28 and W50 induced abscesses at distant sites in both mice and rats. Local lesions were seen in rats injected with strain 381, whereas lesions formed distant from the site of injection in mice. When periodontal bone loss was assessed in the experimental rat model, animals challenged with 33277 had the highest amount of horizontal and vertical bone loss. Rats challenged with strain A7A1-28, W50 or 381 had some or no periodontal bone loss compared with controls. Assessment of antibody responses to P. gingivalis in these animals revealed that rats challenged with 33277 had lower levels of serum immunoglobulin G-(IgG) and especially salivary IgA antibody activity than A7A1-28-challenged rats. Serum IgG and in particular salivary IgA anti-P. gingivalis responses were seen in W50- and 381-challenged rats. These results indicate that the ability of P. gingivalis strains to cause abscesses does not relate directly to their periodontal pathogenicity as assessed by periodontal bone loss in the same animal model. The results further suggest the importance of salivary IgA antibody responses in protection against experimental periodontal bone loss after challenge with P. gingivalis.

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Experimental Porphyromonas gingivalis infection in nonimmune athymic BALB/c mice

Cited by 26 publications

References 18 publications

Virulence of Porphyromonas gingivalis is altered by substitution of fimbria gene with different genotype

Virulence of Porphyromonas gingivalis is altered by substitution of fimbria gene with different genotype

Host responses induced by co‐infection with Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in a murine model

Effect of host responses on the pathogenicity of strains of Porphyromonas gingivalis

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