Journal of clinical periodontology · 2012
The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection.
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Polak David, Shapira Lior, Weiss Ervin I, Houri-Haddad Yael
Аннотация
AIM: To evaluate the role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the virulence of the mixed infection in mice.
MATERIALS AND METHODS: Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection.
RESULTS: Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1-0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL-1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis.
CONCLUSIONS: The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.
MATERIALS AND METHODS: Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection.
RESULTS: Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1-0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL-1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis.
CONCLUSIONS: The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.
Предметные рубрики MeSH
Alveolar Bone LossAnimalsBacterial AdhesionBacteriological TechniquesBacteroidaceae InfectionsCoinfectionDiffusion Chambers, CultureFemaleFusobacterium InfectionsFusobacterium nucleatumHost-Pathogen InteractionsInterleukin-1betaLactoseMiceMice, Inbred BALB CPeriodontitisPhagocytosisPorphyromonas gingivalisSuperinfectionTumor Necrosis Factor-alphaVirulenceX-Ray Microtomography