Yoshimura M, Ohara N, Kondo Y, Shoji M, Okano S, Nakano Y, Abiko Y, Nakayama K
Division of Microbiology and Oral Infection, Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Oral Microbiol Immunol. 2008 Oct;23(5):413-8. doi: 10.1111/j.1399-302X.2008.00444.x.
Porphyromonas gingivalis, an oral anaerobic bacterium, is considered a major pathogen for chronic periodontitis. Pathogenic bacteria usually upregulate or downregulate gene expression to combat the protective responses of their hosts.
To determine what protein is regulated when P. gingivalis cells invade host tissues, we analyzed the proteome of P. gingivalis cells that were placed in a mouse subcutaneous chamber by two-dimensional gel electrophoresis and mass spectrometry.
Fourteen proteins were upregulated, while four proteins were downregulated. We focused on three upregulated proteins, PG1089 (DNA-binding response regulator RprY), PG1385 (TPR domain protein), and PG2102 (immunoreactive 61-kDa antigen), and constructed mutant strains that were defective in these proteins. Mouse abscess model experiments revealed that the mutant strain defective in PG1385 was clearly less virulent than the wild-type parent strain.
These results indicate that the PG1385 protein is involved in P. gingivalis virulence and that the method used here is useful when investigating the P. gingivalis proteins responsible for virulence.
牙龈卟啉单胞菌是一种口腔厌氧菌，被认为是慢性牙周炎的主要病原体。致病细菌通常会上调或下调基因表达以对抗宿主的保护反应。
为了确定牙龈卟啉单胞菌细胞侵入宿主组织时哪些蛋白质受到调控，我们通过二维凝胶电泳和质谱分析了置于小鼠皮下腔室中的牙龈卟啉单胞菌细胞的蛋白质组。
14种蛋白质上调，4种蛋白质下调。我们重点研究了3种上调的蛋白质，即PG1089（DNA结合反应调节因子RprY）、PG1385（TPR结构域蛋白）和PG2102（免疫反应性61 kDa抗原），并构建了这些蛋白质有缺陷的突变菌株。小鼠脓肿模型实验表明，PG1385有缺陷的突变菌株的毒力明显低于野生型亲本菌株。
这些结果表明PG1385蛋白与牙龈卟啉单胞菌的毒力有关，并且这里使用的方法在研究牙龈卟啉单胞菌的毒力相关蛋白时很有用。
