本研究利用動物模型 (Kinetic in situ Subcutaneous Chamber Model, KSCM) 觀察不同牙周病菌感染在此一模型所造成之病理變化，紀錄病變部位宿主免疫細胞種類及數目之變化，細菌數目和毒性表現之消長，以及抗體和發炎物質。Pg HG405 單一感染在KSCM 動物模型中造成局部發炎及膿瘍，相反的，Bf 或Fn 細菌本身甚至無法存活於KSCM 中。當Pg 與Fn 共同混合感染於此一動物模型時，所需Pg 之感染劑量可降至原劑量的十分之一。我們數據顯示此一Fn 對Pg 感染的協力作用(Synergism)與細菌間凝集作用有關。另一方面，Bf 在Fn 存在下亦能生存於此一動物模型並引致感染。Fn 對Bf 的協力作用可被外來的營養素所取代。本研究指出當不同牙周病菌混合感染時，所需致病之劑量遠低於單一感染所需之劑量。
A Kinetic in situ Subcutaneous Chamber Model (KSCM) was used in this study for the evaluation of the molecular, cellular and microbial events associated with the host-pathogen interactions. In these studies we have kinetically analyze the pathologic course of events leading to the local abscess formation that characterizes the clinically relevant scenario. In addition to the progress of macroscopical pathologies, the shift and reactions of host immune cell population and the expression of bacterial virulence were kinetically recorded. Pathogenic synergism between Pg and Fn has been demonstrated. Our data showed 1/10 original Pg infected dosage was capable of causing the same pathology in KSCM when co-inoculated with Fn. Both Pg and Bf produce trypsin-like enzyme and sialidase, which are thought to be involved with bacterial virulence and tissue destruction. The current study evaluated the outcomes of monoinfectious challenge with Fn or Bf in the KSCM animals and determined the influences of Fn inoculation on Bf infection, and synergy mechanism of this mixed infection. An exogenous nutrient supply is sufficient to replace the symbiotic effect of Fn on Bf indicating the synergism between these two bacteria is simply a nutritional dependence. We concluded that mixed infection needed far less bacterial dosage to induce infection in our animal model than monoinfection.
