Amano Atsuo
Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan.
J Periodontol. 2003 Jan;74(1):90-6. doi: 10.1902/jop.2003.74.1.90.
Porphyromonas gingivalis is a predominant periodontal pathogen, which expresses a number of potential virulence factors involved in the pathogenesis of periodontitis. Among them, fimbriae are a critical factor to mediate the bacterial interaction with host tissues, which promotes the bacterial adhesion to and invasion of the targeted sites. Fimbriae are capable of binding to human salivary components, commensal bacteria, and a variety of host cells including macrophages, epithelial cells, and fibroblasts. Human extracellular matrix (ECM) proteins such as vitronectin and fibronectin play important roles in cellular signal transduction via binding to receptor integrins. Fimbriae showed significant binding affinity to ECM proteins and clearly inhibited the molecular interactions between vitronectin/fibronectin and their receptor alphavbeta3 and alpha5beta1 integrins overexpressed on Chinese hamster ovary (CHO) cell strain. P. gingivalis fimbriae are likely to interrupt the cellular signaling via ECM proteins/integrins in periodontal regions. Fimbriae are also thought to be critically important in invasive events of the organism to host cells. The fimA genes, encoding FimA (a subunit of fimbriae), of P. gingivalis strains are classified into 5 types, I to V. Recent clinical investigations demonstrated the close relationship between the organisms with type II fimA and periodontitis development. Recombinant FimA (rFimA) proteins of types I to V were generated to compare their adhesion/invasion abilities to human gingival fibroblasts (HGF) and a human epithelial cell line (HEp-2 cells), respectively. There were no significant differences in the adhesion ability of microspheres (MS) coated with these rFimAs to HGF; however, the adhesion of type II rFimA-MS to HEp-2 cells was significantly greater than that of other rFimA types. It was also observed that the type II rFimA-MS markedly invaded the epithelial cells and accumulated around the nuclei. Collectively, these findings suggest that fimbriae of P. gingivalis, especially type II, are involved in the initiation and progression of human periodontitis.
牙龈卟啉单胞菌是一种主要的牙周病原体,它表达多种参与牙周炎发病机制的潜在毒力因子。其中,菌毛是介导细菌与宿主组织相互作用的关键因素,可促进细菌对靶位点的黏附和侵袭。菌毛能够与人唾液成分、共生细菌以及包括巨噬细胞、上皮细胞和成纤维细胞在内的多种宿主细胞结合。人细胞外基质(ECM)蛋白如玻连蛋白和纤连蛋白通过与受体整合素结合在细胞信号转导中发挥重要作用。菌毛对ECM蛋白表现出显著的结合亲和力,并明显抑制了玻连蛋白/纤连蛋白与其在中国仓鼠卵巢(CHO)细胞株上过表达的受体αvβ3和α5β1整合素之间的分子相互作用。牙龈卟啉单胞菌菌毛可能会通过牙周区域的ECM蛋白/整合素中断细胞信号传导。菌毛在该生物体对宿主细胞的侵袭过程中也被认为至关重要。牙龈卟啉单胞菌菌株编码菌毛亚基FimA的fimA基因分为I至V 5种类型。最近的临床研究表明,具有II型fimA的生物体与牙周炎发展之间存在密切关系。分别产生了I至V型的重组FimA(rFimA)蛋白,以比较它们对人牙龈成纤维细胞(HGF)和人上皮细胞系(HEp-2细胞)的黏附/侵袭能力。包被这些rFimA的微球(MS)对HGF的黏附能力没有显著差异;然而,II型rFimA-MS对HEp-2细胞的黏附明显大于其他rFimA类型。还观察到II型rFimA-MS显著侵袭上皮细胞并在细胞核周围聚集。总体而言,这些发现表明牙龈卟啉单胞菌的菌毛,尤其是II型菌毛,参与了人类牙周炎的发生和发展。