Lamont R J, Jenkinson H F
Department of Oral Biology, University of Washington, Seattle, Washington 98195, USA.
Microbiol Mol Biol Rev. 1998 Dec;62(4):1244-63. doi: 10.1128/MMBR.62.4.1244-1263.1998.
Porphyromonas gingivalis, a gram-negative anaerobe, is a major etiological agent in the initiation and progression of severe forms of periodontal disease. An opportunistic pathogen, P. gingivalis can also exist in commensal harmony with the host, with disease episodes ensuing from a shift in the ecological balance within the complex periodontal microenvironment. Colonization of the subgingival region is facilitated by the ability to adhere to available substrates such as adsorbed salivary molecules, matrix proteins, epithelial cells, and bacteria that are already established as a biofilm on tooth and epithelial surfaces. Binding to all of these substrates may be mediated by various regions of P. gingivalis fimbrillin, the structural subunit of the major fimbriae. P. gingivalis is an asaccharolytic organism, with a requirement for hemin (as a source of iron) and peptides for growth. At least three hemagglutinins and five proteinases are produced to satisfy these requirements. The hemagglutinin and proteinase genes contain extensive regions of highly conserved sequences, with posttranslational processing of proteinase gene products contributing to the formation of multimeric surface protein-adhesin complexes. Many of the virulence properties of P. gingivalis appear to be consequent to its adaptations to obtain hemin and peptides. Thus, hemagglutinins participate in adherence interactions with host cells, while proteinases contribute to inactivation of the effector molecules of the immune response and to tissue destruction. In addition to direct assault on the periodontal tissues, P. gingivalis can modulate eucaryotic cell signal transduction pathways, directing its uptake by gingival epithelial cells. Within this privileged site, P. gingivalis can replicate and impinge upon components of the innate host defense. Although a variety of surface molecules stimulate production of cytokines and other participants in the immune response, P. gingivalis may also undertake a stealth role whereby pivotal immune mediators are selectively inactivated. In keeping with its strict metabolic requirements, regulation of gene expression in P. gingivalis can be controlled at the transcriptional level. Finally, although periodontal disease is localized to the tissues surrounding the tooth, evidence is accumulating that infection with P. gingivalis may predispose to more serious systemic conditions such as cardiovascular disease and to delivery of preterm infants.
牙龈卟啉单胞菌是一种革兰氏阴性厌氧菌,是严重牙周疾病发生和发展的主要病原体。作为一种机会致病菌,牙龈卟啉单胞菌也可与宿主共生,疾病发作是由于复杂牙周微环境中的生态平衡发生变化所致。它能够黏附于唾液分子、基质蛋白、上皮细胞以及已在牙齿和上皮表面形成生物膜的细菌等可利用的底物,从而促进其在龈下区域的定植。牙龈卟啉单胞菌主要菌毛的结构亚基菌毛蛋白的不同区域可能介导其与所有这些底物的结合。牙龈卟啉单胞菌是一种不分解糖类的微生物,生长需要血红素(作为铁的来源)和肽。它至少产生三种血凝素和五种蛋白酶以满足这些需求。血凝素和蛋白酶基因含有高度保守序列的广泛区域,蛋白酶基因产物的翻译后加工有助于形成多聚体表面蛋白黏附素复合物。牙龈卟啉单胞菌的许多毒力特性似乎是其为获取血红素和肽而进行适应的结果。因此,血凝素参与与宿主细胞的黏附相互作用,而蛋白酶则导致免疫反应效应分子失活并造成组织破坏。除了直接侵袭牙周组织外,牙龈卟啉单胞菌还可调节真核细胞信号转导途径,促使牙龈上皮细胞摄取它。在这个特殊部位,牙龈卟啉单胞菌能够繁殖并影响宿主固有防御的成分。尽管多种表面分子刺激细胞因子和免疫反应的其他参与者产生,但牙龈卟啉单胞菌也可能发挥隐匿作用,使关键免疫介质被选择性灭活。与其严格的代谢需求一致,牙龈卟啉单胞菌的基因表达调控可在转录水平进行控制。最后,尽管牙周疾病局限于牙齿周围组织,但越来越多的证据表明,牙龈卟啉单胞菌感染可能使个体易患更严重的全身性疾病,如心血管疾病和早产。