MURINE HOST RESPONSE TO PORPHYROMONAS GINGIVALIS

牙龈卟啉单胞菌是一种革兰氏阴性细菌， 成人牙周病。老鼠的口腔会被感染 牙龈卟啉单胞菌感染，这种口腔感染引起牙槽骨丢失， 牙周病后遗症。口腔感染也可能诱发其他 免疫性疾病。鼠标提供了一个非常多功能的 用于研究宿主对牙龈卟啉单胞菌的免疫应答的模型。的 小鼠免疫系统已被充分表征，并且具有狭窄的 已经发展出特异性的、遗传上确定的免疫缺陷。的 免疫系统中宿主免疫系统的各个方面的需求 保护或启动和发展的牙槽骨丢失的P。 牙龈炎将通过测量感染和 未受感染的小鼠具有特异性免疫缺陷。局限性口腔感染 可以产生抗原特异性或非特异性免疫刺激， 导致外周效应，包括血清抗体，细胞因子， 某些免疫细胞群的扩增和表面的改变 抗原表达牙龈卟啉单胞菌产生外周 体内宿主应答将通过脾细胞的流式细胞术来确定 小鼠口服感染后。细胞因子的细菌诱导可以 增强淋巴细胞的作用，部分激活无关 抗原这一假设将使用同类品系的小鼠进行检验 其对带有细胞毒性T淋巴细胞的供体细胞产生细胞毒性T淋巴细胞应答， 次要组织相容性抗原，只有当他们接受“帮助”， 第二刺激。初步数据显示，第二次刺激可能是 由口腔感染牙龈卟啉单胞菌提供，因此牙龈卟啉单胞菌可能 会导致移植物抗宿主病这些研究将探讨 导致或抑制牙槽骨损失的宿主反应， 开始阐明局部口腔感染与 对宿主的系统性影响。这种小鼠口腔感染的发展 模型将是有用的，在未来澄清之间的相互作用 两种不相关的免疫反应这种澄清可能会产生 疾病病因学研究的新途径。

Porphyromonas gingivalis is a Gram-negative bacterium associated with human adult periodontal disease. The oral cavities of mice can be infected with P. gingivalis, and such oral infection induces alveolar bone loss, a sequela of periodontal disease. Oral infection may also induce other immunologically-based diseases. The mouse offers an extremely versatile model for the study of the host immune response to P. gingivalis. The murine immune system has been well-characterized and strains with narrowly specific, genetically defined immunodeficiencies have been developed. The requirement for various aspects of the host immune system in the protection from or initiation and progression of alveolar bone loss by P. gingivalis will be determined by measuring bone loss in infected and uninfected mice with specific immunodeficiencies. Localized oral infection may produce antigen specific or nonspecific immune stimulation, which may result in peripheral effects including serum antibody, cytokines, expansion of some immune cell populations and alteration of surface antigen expression. The capacity of P. gingivalis to produce peripheral host responses in vivo will be defined by flow cytometry of splenocytes after oral infection of mice. Bacterial induction of cytokines could amplify the effects of lymphocytes partially activated by unrelated antigens. This hypothesis will be tested using congenic strains of mice which develop a cytotoxic T lymphocyte response to donor cell bearing a minor histocompatibility antigen only when they receive "help" from a second stimulus. Preliminary data suggest that this second stimulus may be provided by oral infection with P. gingivalis, thus P. gingivalis might contribute to graft versus host disease. These studies will thus examine the host response leading to or inhibiting alveolar bone loss and will begin to elucidate the relationship between local oral infection and systemic effects in the host. Development of this murine oral infection model will be useful in the future for clarifying the interaction between two unrelated immune responses. Such clarification is likely to produce new avenues of investigation of disease etiology.