Study on the oxidative stress responses of a major periodontopathogenic bacteria

一种主要牙周病原菌氧化应激反应的研究

基本信息

  • 批准号:
    16591831
  • 负责人:
  • 金额:
    $ 2.3万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2004
  • 资助国家:
    日本
  • 起止时间:
    2004 至 2005
  • 项目状态:
    已结题

项目摘要

Inspection of genomic DNA sequence of the oral anaerobe Porphyromonas gingivalis reveals that the microorganism possesses the peroxide-sensing transcription activator OxyR, but not the superoxide-sensing transcription factor SoxR. Oxidative stress-responsive proteins in the microorganism were investigated using two dimensional gel electrophoresis and it was found that two proteins, SOD and AhpC were predominantly upregulated in oxidative conditions. In P. gingivalis oxyR mutant these two proteins were not induced by treatment with hydrogen peroxide under aerobic conditions. P.gingivalis sod and ahpC were positively regulated by OxyR. Putative -35 boxes of these promoters were found immediately adjacent to their putative OxyR binding sequences. Moreover, the promoter regions of sod and ahpC had the ability to bind P.gingivalis OxyR protein. These results demonstrate that P.gingivalis sod is one of the OxyR regulons, suggesting that OxyR functions as an intracellular redox sensor rather than a peroxide sensor in this organism.The new protein (UstA) was also identified in this study. Expression of UstA was upregulated in stationary phase or by exposure to atmospheric oxygen. The UstA-encoding gene (ustA) was located upstream of a homologue of the usp gene. The ustA gene appeared to be transcribed in a monocistronic fashion. The ustA mutant grew slower than the wild type parent strain, resulting in a lower yield in stationary phase. Furthermore, in this mutant, the expression levels of SOD, Tpr, and Trx were markedly higher than those in the wild type. The ustA mutant was more resistant to diamide, a thiol-specific oxidant, than the wild type. In addition, the ustA mutation suppressed hypersensitivities of the oxyR mutant to diamide,. metronidazole, and mitomycin C. These results suggest that UstA may play a significant role in oxidative stress responses in the bacterium.
对口腔厌氧斑点牙龈的基因组DNA序列的检查表明,微生物具有过氧化物敏感性转录激活剂oxyr,但没有超氧化物感应转录因子SOXR。使用二维凝胶电泳研究了微生物中的氧化应激反应性蛋白,发现在氧化条件下,两种蛋白质,SOD和AHPC主要上调。在牙龈疟原虫氧气突变体中,这两种蛋白质未通过有氧条件下用过氧化氢处理诱导。 P.ganivalis SOD和AHPC受Oxyr的正面调节。假定的-35盒这些启动子被发现与假定的Oxyr结合序列相邻。此外,SOD和AHPC的启动子区域具有结合oxyris oxyr蛋白的能力。这些结果表明,吉维尔斯SOD是Oxyr调节子之一,表明Oxyr在该生物体中充当细胞内氧化还原传感器而不是过氧化物传感器。在这项研究中,新蛋白(USTA)也被鉴定出来。 USTA的表达在固定相或暴露于大气中的氧气上上调。 USTA编码基因(USTA)位于USP基因同源物的上游。 USTA基因似乎以单科式的方式转录。 USTA突变体的增长速度比野生型母体应变慢,导致固定相的产率较低。此外,在这个突变体中,SOD,TPR和TRX的表达水平明显高于野生型的表达水平。与野生型相比,USTA突变体对二酰胺(一种硫醇特异性氧化剂)更具抵抗力。另外,USTA突变抑制了氧远变的超敏反应为二酰胺。甲硝唑和丝霉素C.这些结果表明USTA可能在细菌中的氧化应激反应中起重要作用。

项目成果

期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
The novel stationary-phase-upregulated protein of Porphyromonas gingivalis influences the production of superoxide dismutase, thiol peroxidase and thioredoxin.
牙龈卟啉单胞菌的新型稳定期上调蛋白影响超氧化物歧化酶、硫醇过氧化物酶和硫氧还蛋白的产生。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Matsumoto S;Kanekiyo M;Ami Y;Oiso R;松本 壮吉;松本 壮吉;Zhang Z;Soejima H;Arima T;Yamasaki Y;Soejima H;Haruta M;副島英伸;Naoya Ohara;Marika Naito;Yuichiro Kikuchi
  • 通讯作者:
    Yuichiro Kikuchi
Novel stationary-phase-upregulated protein of Porphyromonas gingivalis influences production of superoxide dismutase, thiol peroxidase and thioredoxin
  • DOI:
    10.1099/mic.0.27589-0
  • 发表时间:
    2005-03-01
  • 期刊:
  • 影响因子:
    2.8
  • 作者:
    Kikuchi, Y;Ohara, N;Nakayama, K
  • 通讯作者:
    Nakayama, K
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OHARA Naoya其他文献

Mycobacterial infection induces eosinophilia and production of α-defensin by eosinophils in mice
分枝杆菌感染诱导小鼠嗜酸性粒细胞增多和嗜酸性粒细胞产生α-防御素
  • DOI:
    10.1292/jvms.18-0619
  • 发表时间:
    2019
  • 期刊:
  • 影响因子:
    1.2
  • 作者:
    KHATUN Afia;SAKURAI Masashi;SAKAI Yusuke;TACHIBANA Masato;OHARA Naoya;MORIMOTO Masahiro
  • 通讯作者:
    MORIMOTO Masahiro

OHARA Naoya的其他文献

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{{ truncateString('OHARA Naoya', 18)}}的其他基金

Understanding the pathogenicity of periodontal disease onset and systemic disease exacerbation caused by periodontal bacteria
了解牙周细菌引起的牙周病发病和全身性疾病恶化的致病性
  • 批准号:
    17H04378
  • 财政年份:
    2017
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Molecular mechanisms of periodontal diseases and systematic diseases associated with periodontal diseases by periodontal pathogens
牙周病原菌引起的牙周病及与牙周病相关的系统性疾病的分子机制
  • 批准号:
    26293401
  • 财政年份:
    2014
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Study on the survival strategies for periodontal bacteria in host cells and their role in the pathogenesis of periodontal diseases
牙周细菌在宿主细胞内的生存策略及其在牙周病发病机制中的作用研究
  • 批准号:
    22390342
  • 财政年份:
    2010
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of molecular mechanism of bone metabolism disruption by bacterial infection
细菌感染破坏骨代谢的分子机制分析
  • 批准号:
    19592118
  • 财政年份:
    2007
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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牙龈卟啉单胞菌逃逸异源自噬致牙周炎症的效应和机制研究
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