Nagata Hideki, Iwasaki Mio, Maeda Kazuhiko, Kuboniwa Masae, Hashino Ei, Toe Masahiro, Minamino Naoto, Kuwahara Hiromiki, Shizukuishi Satoshi
Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan.
Infect Immun. 2009 Nov;77(11):5130-8. doi: 10.1128/IAI.00439-09. Epub 2009 Sep 8.
Porphyromonas gingivalis forms communities with antecedent oral biofilm constituent streptococci. P. gingivalis major fimbriae bind to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) present on the streptococcal surface, and this interaction plays an important role in P. gingivalis colonization. This study identified the binding domain of Streptococcus oralis GAPDH for P. gingivalis fimbriae. S. oralis recombinant GAPDH (rGAPDH) was digested with lysyl endopeptidase. Cleaved fragments of rGAPDH were applied to a reverse-phase high-pressure liquid chromatograph equipped with a C18 column. Each peak was collected; the binding activity toward P. gingivalis recombinant fimbrillin (rFimA) was analyzed with a biomolecular interaction analysis system. The fragment displaying the strongest binding activity was further digested with various proteinases, after which the binding activity of each fragment was measured. The amino acid sequence of each fragment was determined by direct sequencing, mass spectrometric analysis, and amino acid analysis. Amino acid residues 166 to 183 of S. oralis GAPDH exhibited the strongest binding activity toward rFimA; confocal laser scanning microscopy revealed that the synthetic peptide corresponding to amino acid residues 166 to 183 of S. oralis GAPDH (pep166-183, DNFGVVEGLMTTIHAYTG) inhibits S. oralis-P. gingivalis biofilm formation in a dose-dependent manner. Moreover, pep166-183 inhibited interbacterial biofilm formation by several oral streptococci and P. gingivalis strains with different types of FimA. These results indicate that the binding domain of S. oralis GAPDH for P. gingivalis fimbriae exists within the region encompassing amino acid residues 166 to 183 of GAPDH and that pep166-183 may be a potent inhibitor of P. gingivalis colonization in the oral cavity.
牙龈卟啉单胞菌与先前存在的口腔生物膜成分链球菌形成群落。牙龈卟啉单胞菌的主要菌毛与存在于链球菌表面的甘油醛-3-磷酸脱氢酶(GAPDH)结合,这种相互作用在牙龈卟啉单胞菌的定植中起重要作用。本研究确定了口腔链球菌GAPDH与牙龈卟啉单胞菌菌毛的结合结构域。用赖氨酰内肽酶消化口腔链球菌重组GAPDH(rGAPDH)。将rGAPDH的裂解片段应用于配备C18柱的反相高压液相色谱仪。收集每个峰;用生物分子相互作用分析系统分析其对牙龈卟啉单胞菌重组菌毛蛋白(rFimA)的结合活性。对显示最强结合活性的片段用各种蛋白酶进一步消化,然后测定每个片段的结合活性。通过直接测序、质谱分析和氨基酸分析确定每个片段的氨基酸序列。口腔链球菌GAPDH的166至183位氨基酸残基对rFimA表现出最强的结合活性;共聚焦激光扫描显微镜显示,对应于口腔链球菌GAPDH 166至183位氨基酸残基的合成肽(pep166-183,DNFGVVEGLMTTIHAYTG)以剂量依赖方式抑制口腔链球菌-牙龈卟啉单胞菌生物膜形成。此外,pep166-183抑制几种口腔链球菌和具有不同类型FimA的牙龈卟啉单胞菌菌株之间的细菌间生物膜形成。这些结果表明,口腔链球菌GAPDH与牙龈卟啉单胞菌菌毛的结合结构域存在于GAPDH的166至18氨基酸残基区域内,并且pep166-183可能是口腔中牙龈卟啉单胞菌定植的有效抑制剂。