Search

Porphyromonas gingivalis and Treponema denticola are major pathogens of periodontal disease. Coaggregation between microorganisms plays a key role in the colonization of the gingival crevice and the organization of periodontopathic biofilms. We investigated the involvement of surface ligands of P. gingivalis in coaggregation. Two triple mutants of P. gingivalis lacking Arg-gingipain A (RgpA), Lys-gingipain (Kgp) and Hemagglutinin A (HagA) or RgpA, Arg-gingipain B (RgpB) and Kgp showed significantly decreased coaggregation with T. denticola, whereas coaggregation with a major fimbriae (FimA)-deficient mutant was the same as that with the P. gingivalis wild-type parent strain. rgpA, kgp and hagA code for proteins that contain 44 kDa Hgp44 adhesin domains. The coaggregation activity of an rgpA kgp mutant was significantly higher than that of the rgpA kgp hagA mutant. Furthermore, anti-Hgp44 immunoglobulin G reduced coaggregation between P. gingivalis wild type and T. denticola. Treponema denticola sonicates adhered to recombinant Rgp domains. Coaggregation following co-culture of the rgpA kgp hagA mutant expressing the RgpB protease with the rgpA rgpB kgp mutant expressing the unprocessed HagA protein was enhanced compared with that of each triple mutant with T. denticola. These results indicate that the processed P. gingivalis surface Hgp44 domains are key adhesion factors for coaggregation with T. denticola. [ABSTRACT FROM AUTHOR]

Galectins, a family of animal lectins, are involved not only in development and differentiation but also in immunoregulation and host–pathogen interactions. Galectin-3 interacts with lipopolysaccharides in gram-negative bacteria such as Escherichia coli, Salmonella minnesota and Pseudomonas aeruginosa. The present study investigated whether galectin-3 inhibited the cytokine-inducing activity of periodontopathic bacterial lipopolysaccharides using splenocytes derived from mice of different ages. Lipopolysaccharides were extracted from Aggregatibacter actinomycetemcomitans Y4 and Porphyromonas gingivalis ATCC 33277, and then purified. Enzyme-linked immunosorbent assay (ELISA) analysis revealed that galectin-3 adhered to A. actinomycetemcomitans lipopolysaccharides, but not to the lipopolysaccharides of P. gingivalis. Splenocytes were prepared from 1- or 7-month-old C57BL/6 mice. Either A. actinomycetemcomitans lipopolysaccharides (200 ng mL−1) alone or lipopolysaccharides and murine galectin-3 (10 μg mL−1) were added to culture solutions, and the release of interleukin-6 (IL-6) and interferon-γ (IFNγ) from splenocytes was measured by ELISA after a 17-h incubation. In all mice tested, A. actinomycetemcomitans lipopolysaccharide stimulation significantly increased the production of IL-6 and IFNγ ( P<0.01). Murine galectin-3 suppressed lipopolysaccharide-induced cytokine production in the splenocytes of the 1-month-old mice ( P<0.02 for IL-6; P<0.05 for IFNγ), but not in the splenocytes of the 7-month-old mice. This suggests that responses change with age. [ABSTRACT FROM AUTHOR]

Invasion by Porphyromonas gingivalis has been proposed as a possible mechanism of pathogenesis in periodontal and cardiovascular diseases. Porphyromonas gingivalis have direct access to the systemic circulation and endothelium in periodontitis patients by transient bacteremia. Periodontitis can be described as one of the predominant polymicrobial infections of humans. In the present study, P. gingivalis strains were tested for their ability to invade a human gingival epithelial cell line (Ca9-22) and human aortic endothelial cells in coinfection with Fusobacterium nucleatum using antibiotic protection assays. Coinfection with F. nucleatum resulted in 2–20-fold increase in the invasion of host cells by P. gingivalis strains. The invasive abilities of P. gingivalis strains were significantly greater when incubated with a F. nucleatum clinical isolate (which possesses strong biofilm-forming ability), than when incubated with a F. nucleatum-type strain. In inhibition assays with metabolic inhibitors, a difference in inhibition profiles was observed between mono- and polymicrobial infections. Collectively, our results suggest that F. nucleatum facilitates invasion of host cells by P. gingivalis. Investigations of polymicrobial infection of host cells should improve our understanding of the role of P. gingivalis in periodontal infection and proatherogenic mechanisms. [ABSTRACT FROM AUTHOR]

We studied the effect of antibodies against Porphyromonas gingivalis gingipain domains, preparing them against three recombinant fragments of RgpA (catalytic domain, r-Rgp CAT; hemagglutinin domains, r-Rgp 44 and r-Rgps 15–27) and one fragment of Kgp (catalytic domain, r-Kgp CAT). Enhancement of opsonization and killing by human polymorphonuclear leukocytes were measured in the noninvasive FDC 381 and invasive W50 strains of P. gingivalis. Anti-r-Rgp 44 was the most effective in both strains of P. gingivalis. The present findings lead us to recommend RgpA 44 as a candidate immunogen for vaccines against P. gingivalis. [ABSTRACT FROM AUTHOR]