Tamai Riyoko, Asai Yasuyuki, Ogawa Tomohiko
Department of Oral Microbiology, Asahi University School of Dentistry, Mizuho, Gifu, Japan.
Infect Immun. 2005 Oct;73(10):6290-8. doi: 10.1128/IAI.73.10.6290-6298.2005.
Porphyromonas gingivalis, a periodontopathic bacterium, is known to invade oral epithelial cells in periodontal lesions, although the mechanism is unclear. In the present study, goat polyclonal anti-intercellular adhesion molecule 1 (anti-ICAM-1) antibody inhibited the invasion of P. gingivalis into KB cells (human oral epithelial cells). Further, the P. gingivalis fimbria, a pathogenic adhesion molecule, bound to recombinant human ICAM-1, as shown by enzyme-linked immunosorbent assay. P. gingivalis was also found to colocalize with ICAM-1 on KB cells, as seen with an immunofluorescence microscope, and the knockdown of ICAM-1 in KB cells resulted in the inhibition of P. gingivalis invasion by RNA interference. In addition, methyl-beta-cyclodextrin, a cholesterol-binding agent, inhibited the colocalization of P. gingivalis with ICAM-1 and invasion by the microorganism. The colocalization of caveolin-1, a caveolar marker protein, on KB cells with P. gingivalis was also shown, and the knockdown of caveolin-1 in KB cells caused a reduced level of P. gingivalis invasion. These results suggest that ICAM-1 and caveolae are required for the invasion of P. gingivalis into human oral epithelial cells, and these molecules appear to be associated with the primary stages of the development and progression of chronic periodontitis.
牙龈卟啉单胞菌是一种牙周病原菌,已知其可侵入牙周病变中的口腔上皮细胞,但其机制尚不清楚。在本研究中,山羊抗细胞间黏附分子1(抗ICAM - 1)多克隆抗体抑制了牙龈卟啉单胞菌对KB细胞(人口腔上皮细胞)的侵袭。此外,酶联免疫吸附测定表明,牙龈卟啉单胞菌的菌毛(一种致病性黏附分子)与重组人ICAM - 1结合。用免疫荧光显微镜观察发现,牙龈卟啉单胞菌也与KB细胞上的ICAM - 1共定位,并且KB细胞中ICAM - 1的敲低通过RNA干扰导致牙龈卟啉单胞菌侵袭受到抑制。此外,胆固醇结合剂甲基 - β - 环糊精抑制了牙龈卟啉单胞菌与ICAM - 1的共定位以及该微生物的侵袭。还显示了小窝标记蛋白小窝蛋白 - 1在KB细胞上与牙龈卟啉单胞菌的共定位,并且KB细胞中小窝蛋白 - 1的敲低导致牙龈卟啉单胞菌侵袭水平降低。这些结果表明,ICAM - 1和小窝对于牙龈卟啉单胞菌侵入人口腔上皮细胞是必需的,并且这些分子似乎与慢性牙周炎发生和发展的初级阶段相关。