Sakai Eiko, Naito Mariko, Sato Keiko, Hotokezaka Hitoshi, Kadowaki Tomoko, Kamaguchi Arihide, Yamamoto Kenji, Okamoto Kuniaki, Nakayama Koji
Department of Developmental and Reconstructive Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Sakamoto 1-7-1, Nagasaki 852-8588, Japan.
J Bacteriol. 2007 Jun;189(11):3977-86. doi: 10.1128/JB.01691-06. Epub 2007 Mar 23.
Porphyromonas gingivalis, an anaerobic gram-negative bacterium associated with chronic periodontitis, can agglutinate human erythrocytes. In general, hemagglutination can be considered the ability to adhere to host cells; however, P. gingivalis-mediated hemagglutination has special significance because heme markedly accelerates growth of this bacterium. Although a number of studies have indicated that a major hemagglutinin of P. gingivalis is intragenically encoded by rgpA, kgp, and hagA, direct evidence has not been obtained. We demonstrated in this study that recombinant HGP44(720-1081), a fully processed HGP44 domain protein, had hemagglutinating activity but that an unprocessed form, HGP44(720-1138), did not. A peptide corresponding to residues 1083 to 1102, which was included in HGP44(720-1138) but not in HGP44(720-1081), could bind HGP44(720-1081) in a dose-dependent manner and effectively inhibited HGP44(720-1081)-mediated hemagglutination, indicating that the interdomain regional amino acid sequence may function as an intramolecular suppressor of hemagglutinating activity. Analyses by solid-phase binding and chemical cross-linking suggested that HGP44 interacted with glycophorin A on the erythrocyte membrane. Glycophorin A and, more effectively, asialoglycophorin, which were added exogenously, inhibited HGP44(720-1081)-mediated hemagglutination. Treatment of erythrocytes with RgpB proteinase resulted in degradation of glycophorin A on the membrane and a decrease in HGP44(720-1081)-mediated hemagglutination. Surface plasmon resonance detection analysis revealed that HGP44(720-1081) could bind to asialoglycophorin with a dissociation constant of 3.0 x 10(-7) M. These results indicate that the target of HGP44 on the erythrocyte membrane appears to be glycophorin A.
牙龈卟啉单胞菌是一种与慢性牙周炎相关的革兰氏阴性厌氧菌,它能够凝集人红细胞。一般来说,血细胞凝集可被视为一种粘附宿主细胞的能力;然而,牙龈卟啉单胞菌介导的血细胞凝集具有特殊意义,因为血红素能显著加速该细菌的生长。尽管多项研究表明牙龈卟啉单胞菌的主要血细胞凝集素由rgpA、kgp和hagA基因内编码,但尚未获得直接证据。我们在本研究中证明,重组HGP44(720 - 1081),一种完全加工的HGP44结构域蛋白,具有血细胞凝集活性,而未加工形式的HGP44(720 - 1138)则没有。一个对应于1083至1102位残基的肽段,它包含在HGP44(720 - 1138)中但不包含在HGP44(720 - 1081)中,能够以剂量依赖的方式结合HGP44(720 - 1081),并有效抑制HGP44(720 - 1081)介导的血细胞凝集,这表明结构域间区域的氨基酸序列可能作为血细胞凝集活性的分子内抑制剂发挥作用。通过固相结合和化学交联分析表明,HGP44与红细胞膜上的血型糖蛋白A相互作用。外源添加的血型糖蛋白A,以及更有效的去唾液酸血型糖蛋白,抑制了HGP44(720 - 1081)介导的血细胞凝集。用RgpB蛋白酶处理红细胞导致膜上血型糖蛋白A降解,HGP44(720 - 1081)介导的血细胞凝集减少。表面等离子体共振检测分析显示,HGP44(720 - 1081)能够以3.0×10(-7)M的解离常数与去唾液酸血型糖蛋白结合。这些结果表明,红细胞膜上HGP44的靶点似乎是血型糖蛋白A。