Role of Superoxide Dismutase in the Resistance of Periodontopathic Bacteria to Killing by Neutrophils

超氧化物歧化酶在牙周病细菌抵抗中性粒细胞杀灭中的作用

基本信息

  • 批准号:
    02454469
  • 负责人:
  • 金额:
    $ 4.35万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
  • 财政年份:
    1990
  • 资助国家:
    日本
  • 起止时间:
    1990 至 1991
  • 项目状态:
    已结题

项目摘要

In this study, we assessed the influence of superoxide dismutase, which was varied by inducing its synthesis or by adding it exogenously, on killing of black-pigmented oral anaerobic rods by neutrophils. Porphyromonas gingivalis 381 which had a high SOD activity was not highly sensitive to the killing effect of neutrophils. However, Prevotella denticola ATCC 33185 which showed the lowest activity of SOD and was also the highest oxygen sensitivity among the black-pigmented oral anaerobic rods tested was immediately killed after phagocytosis.SOD_s were purified from extracts of either anaerobically maintained or aerated P. gingivalis 381 (anaers-SOD and aero-SOD, respectively). Each-purified enzyme showed same molecular weight and isoelectric points. Furthermore, the two enzymes had completely identical amino acid, -sequences. However, metal contents and spectral analysis of both enzymes showed that anaers-SOD had the characteristic of FE-SOD and that aero-SOD had that of MnSOD. The effect of aero-SOD or anaers-SOD added exogenously on resistance of P. gingivalis to killing by neutrophils was examined. Both SOD_s inhibited bacterial killing, but there was no difference in the inhibitory effects between these two enzymes.Induction of the synthesis of SOD in P. gingivalis 381 was performed by an aeration or by the addition of potassium nitrate to the growth medium. When the specific activities of SOD in P. gingivalis 381 increased 2.3-fold and 2.0-fold by growth in the presence of nitrate and by aeration, respectively, the resistances of the bacterium to killing by the neutrophils were significantly greater than that of control. These results suggest that SOD may form part of a defence mechanism that helps protect P. gingivalis from killing by neutrophils.
在本研究中,我们评估了超氧化物歧化酶对中性粒细胞杀死黑色口腔厌氧棒的影响,该酶通过诱导其合成或外源添加而变化。SOD活性较高的牙龈卟啉单胞菌381对中性粒细胞的杀伤作用不敏感。而在黑色口腔厌氧棒中SOD活性最低、氧敏感性最高的齿状普雷沃特菌ATCC 33185被吞噬后立即死亡。分别从厌氧维持或曝气的牙龈假单胞菌381的提取物中纯化出SOD_s(厌氧sod和曝气sod)。纯化后的酶具有相同的分子量和等电点。此外,这两种酶具有完全相同的氨基酸-序列。然而,两种酶的金属含量和光谱分析表明,厌氧sod具有FE-SOD的特征,而气动sod具有MnSOD的特征。研究了外源添加的aero-SOD和anaers-SOD对牙龈卟啉单胞菌抗中性粒细胞杀伤的影响。两种SOD_s对细菌杀灭均有抑制作用,但两种酶的抑制作用没有差异。通过曝气或在培养基中添加硝酸钾诱导牙龈卟啉卟啉381合成SOD。当P. gingivalis 381在硝酸盐和曝气条件下的SOD比活性分别提高2.3倍和2.0倍时,细菌对中性粒细胞杀伤的抵抗力显著高于对照。这些结果表明,SOD可能是一种防御机制的一部分,有助于保护牙龈卟啉卟啉菌免受中性粒细胞的杀伤。

项目成果

期刊论文数量(25)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Atsuo Amano el al.: "The primary structure of superoxide dismutase purified from anaerobically maintained Bacteroides gingivalis." FEBS Lett. 272. 217-220 (1990)
Atsuo Amano 等人:“从厌氧维持的牙龈拟杆菌中纯化的超氧化物歧化酶的一级结构。”
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    0
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Atsuo Amano: "Role of superoxide dismutase in the resistance of Porphyromonas gingivalis to killing by polymorphonuclear leukocytes" Infect.Immun.60. (1992)
Atsuo Amano:“超氧化物歧化酶在抵抗多形核白细胞杀伤牙龈卟啉单胞菌中的作用”Infect.Immun.60。
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Atsuo Amano: "The primary structure of superoxide dismutase purified from anaerobically maintained <Bacteroides gingivalis>___ー" FEBS Letters. 272. 217-220 (1990)
Atsuo Amano:“从厌氧维持的<牙龈拟杆菌>中纯化的超氧化物歧化酶的一级结构___”FEBS Letters 272. 217-220 (1990)。
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    0
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Atsuo Amano et al.: "Role of P. gingivalis superoxide dismutase in resistance to killing by neutrophils." J. Dent. Res.70. 1211 (1991)
Atsuo Amano 等人:“牙龈卟啉单胞菌超氧化物歧化酶在抵抗中性粒细胞杀伤作用中的作用。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Atsuo Amano: "The primary structure of superoxide dismutase purified from anaerobically maintained Bacteroides gingivalis" FEBS Letters. 272. 217-220 (1990)
Atsuo Amano:“从厌氧维持的牙龈拟杆菌中纯化的超氧化物歧化酶的一级结构”FEBS Letters。
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SHIZUKUISHI Satoshi其他文献

SHIZUKUISHI Satoshi的其他文献

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{{ truncateString('SHIZUKUISHI Satoshi', 18)}}的其他基金

Molecular mechanism involved in the association of periodontal disease with pathology of metabolic syndrome
牙周病与代谢综合征病理关联的分子机制
  • 批准号:
    19209064
  • 财政年份:
    2007
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Elucidation of molecular mechanism of binding between periodontopathic bacteria and oral streptococci, and development of agents which inhibit forming of dental biofilm
阐明牙周病细菌与口腔链球菌结合的分子机制,开发抑制牙齿生物膜形成的药物
  • 批准号:
    17390564
  • 财政年份:
    2005
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Development of effective immunization by DNA vaccine against iron-acquisition protein of periodontopathic bacteria
DNA疫苗开发针对牙周病细菌铁获取蛋白的有效免疫
  • 批准号:
    14370694
  • 财政年份:
    2002
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Development of New Oral Health Practice Index Based on Lifestyle and Oral Health Age
基于生活方式和口腔健康年龄的新口腔健康实践指数的开发
  • 批准号:
    12557183
  • 财政年份:
    2000
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Biomolecular analysis on iron acquisition mechanism and pathogenicity of periodontopathic bacteria
牙周病细菌铁获取机制及致病性的生物分子分析
  • 批准号:
    11307050
  • 财政年份:
    1999
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Development of inhibitory peptide in oral bacterial coaggregation
口腔细菌共凝抑制肽的开发
  • 批准号:
    09044302
  • 财政年份:
    1997
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for international Scientific Research
Development of inhibitory peptide in adherence of periodontopathic bacteria to dental plaqu
牙周病细菌粘附牙菌斑抑制肽的研制
  • 批准号:
    09557175
  • 财政年份:
    1997
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of structure and function of saliva protein receptor domains for periodontopathogen
牙周病原唾液蛋白受体结构域结构与功能分析
  • 批准号:
    08457568
  • 财政年份:
    1996
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Development of Smoking Cessation Training Program for Dental Team
牙科团队戒烟培训计划的制定
  • 批准号:
    07557285
  • 财政年份:
    1995
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
MECHANISMS OF IRON-A CQUISITION FROM HEMOGLOBIN IN PORPHYROMONAS GINGIVALIS
从牙龈卟啉单胞菌血红蛋白中获取铁的机制
  • 批准号:
    05454555
  • 财政年份:
    1993
  • 资助金额:
    $ 4.35万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)

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CAREER: Oligomeric Stoichiometry of Superoxide Dismutase 1 and Neuronal Antioxidant Defense
职业:超氧化物歧化酶 1 的寡聚化学计量和神经元抗氧化防御
  • 批准号:
    2237129
  • 财政年份:
    2023
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    $ 4.35万
  • 项目类别:
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Determining the role of Reactive Oxygen Species (ROS) and Superoxide dismutase 1 (Sod1) in lung cancer and melanoma development
确定活性氧 (ROS) 和超氧化物歧化酶 1 (Sod1) 在肺癌和黑色素瘤发展中的作用
  • 批准号:
    486141
  • 财政年份:
    2022
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    $ 4.35万
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    Studentship Programs
Deciphering the Enzymatic Mechanism of Superoxide Dismutase
破译超氧化物歧化酶的酶促机制
  • 批准号:
    10663311
  • 财政年份:
    2022
  • 资助金额:
    $ 4.35万
  • 项目类别:
Deciphering the Enzymatic Mechanism of Superoxide Dismutase
破译超氧化物歧化酶的酶促机制
  • 批准号:
    10418479
  • 财政年份:
    2022
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  • 项目类别:
Deciphering the Enzymatic Mechanism of Superoxide Dismutase
破译超氧化物歧化酶的酶促机制
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    10797963
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Leveraging host-imposed metal starvation to elucidate the molecular and environmental factors that dictate metal utilization by the iron/manganese superoxide dismutase superfamily
利用宿主施加的金属饥饿来阐明决定铁/锰超氧化物歧化酶超家族利用金属的分子和环境因素
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    10294718
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    2021
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Leveraging host-imposed metal starvation to elucidate the molecular and environmental factors that dictate metal utilization by the iron/manganese superoxide dismutase superfamily
利用宿主施加的金属饥饿来阐明决定铁/锰超氧化物歧化酶超家族利用金属的分子和环境因素
  • 批准号:
    10407651
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Selective delivery of superoxide dismutase and catalase for restenosis prevention
选择性递送超氧化物歧化酶和过氧化氢酶以预防再狭窄
  • 批准号:
    10514528
  • 财政年份:
    2021
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    $ 4.35万
  • 项目类别:
Leveraging host-imposed metal starvation to elucidate the molecular and environmental factors that dictate metal utilization by the iron/manganese superoxide dismutase superfamily
利用宿主施加的金属饥饿来阐明决定铁/锰超氧化物歧化酶超家族利用金属的分子和环境因素
  • 批准号:
    10617269
  • 财政年份:
    2021
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    $ 4.35万
  • 项目类别:
Selective delivery of superoxide dismutase and catalase for restenosis prevention
选择性递送超氧化物歧化酶和过氧化氢酶以预防再狭窄
  • 批准号:
    10315701
  • 财政年份:
    2021
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