MURINE HOST RESPONSE TO PORPHYROMONAS GINGIVALIS

牙龈卟啉单胞菌是一种革兰氏阴性细菌，与 成人牙周病。小鼠的口腔可以被感染 这种口腔感染会导致牙槽骨丢失， 牙周病的后遗症。口腔感染也可能导致其他 免疫学疾病。鼠标提供了一种非常通用的 研究牙龈假单胞菌宿主免疫反应的模型。这个 小鼠的免疫系统已经有了很好的特征，并且菌株之间的差距很小 特定的、基因定义的免疫缺陷已经被开发出来。这个 对宿主免疫系统的各个方面的要求 P。对牙槽骨丢失的保护作用或开始和进展。 将通过测量感染和感染的患者的骨丢失来确定牙周炎 具有特定免疫缺陷的未感染小鼠。局限性口腔感染 可能产生抗原特异性或非特异性免疫刺激，这可能 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。牙周炎假单胞菌产生外周血细胞的能力 体内宿主反应将通过脾细胞的流式细胞术来确定 小鼠口服感染后。细菌对细胞因子的诱导可能 放大非亲缘关系部分激活淋巴细胞的效应 抗原。这一假说将用同基因品系的小鼠进行检验。 它们对携带A细胞的供体细胞产生细胞毒性T淋巴细胞反应 次要组织相容抗原仅当他们接受来自 第二轮刺激。初步数据显示，第二轮刺激可能是 由口腔感染牙龈假单胞菌提供，因此牙龈假单胞菌可能 导致移植物抗宿主病。因此，这些研究将检查 导致或抑制牙槽骨丢失的宿主反应 开始阐明口腔局部感染与疾病的关系 寄主的全身性影响。这种小鼠口腔感染的发展 该模型将在未来用于阐明 两种互不相关的免疫反应。这样的澄清很可能会产生 疾病病因研究的新途径。

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.