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补体介导的对易感革兰氏阴性菌的杀伤作用:一种难以捉摸的机制。

Complement-mediated killing of susceptible gram-negative bacteria: an elusive mechanism.

作者信息

Taylor P W

机构信息

CIBA-Geigy Pharmaceuticals, Horsham, UK.

出版信息

Exp Clin Immunogenet. 1992;9(1):48-56.

PMID:1642903
Abstract

Exposure of gram-negative bacteria to a source of antibody and complement frequently results in efficient cell killing; this effect follows the deposition of C5b-9 membrane attack complexes onto the bacterial surface. This review examines the molecular and physiological events culminating in C5b-9 deposition and cell death and advances an hypothesis that may account for cytoplasmic-membrane damage following complement-mediated perturbation of the outer membrane.

摘要

革兰氏阴性菌暴露于抗体和补体来源时,常常会导致有效的细胞杀伤;这种效应是在C5b - 9膜攻击复合物沉积到细菌表面之后出现的。本综述研究了最终导致C5b - 9沉积和细胞死亡的分子和生理事件,并提出了一个假说,该假说可能解释补体介导的外膜扰动后细胞质膜的损伤。

相似文献

1
Complement-mediated killing of susceptible gram-negative bacteria: an elusive mechanism.补体介导的对易感革兰氏阴性菌的杀伤作用:一种难以捉摸的机制。
Exp Clin Immunogenet. 1992;9(1):48-56.
2
Complement-mediated killing of the Lyme disease spirochete Borrelia burgdorferi. Role of antibody in formation of an effective membrane attack complex.补体介导的莱姆病螺旋体伯氏疏螺旋体的杀伤作用。抗体在有效膜攻击复合物形成中的作用。
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Studies on the mechanism of bacterial resistance to complement-mediated killing. VI. IgG increases the bactericidal efficiency of C5b-9 for E. coli 0111B4 by acting at a step before C5 cleavage.细菌对补体介导杀伤作用的抗性机制研究。VI. IgG通过在C5裂解前的一个步骤发挥作用,提高C5b-9对大肠杆菌0111B4的杀菌效率。
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Multimeric C9 within C5b-9 is required for inner membrane damage to Escherichia coli J5 during complement killing.补体杀伤过程中,C5b-9内的多聚体C9是对大肠杆菌J5内膜造成损伤所必需的。
J Immunol. 1987 Feb 1;138(3):842-8.
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Studies of the mechanism of bacterial resistance to complement-mediated killing. V. IgG and F(ab')2 mediate killing of E. coli 0111B4 by the alternative complement pathway without increasing C5b-9 deposition.细菌对补体介导杀伤的抗性机制研究。V. IgG和F(ab')2通过替代补体途径介导对大肠杆菌O111B4的杀伤,而不增加C5b-9沉积。
J Immunol. 1983 Nov;131(5):2563-9.
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Studies on the mechanism of bacterial resistance to complement-mediated killing. IV. C5b-9 forms high molecular weight complexes with bacterial outer membrane constituents on serum-resistant but not on serum-sensitive Neisseria gonorrhoeae.细菌对补体介导杀伤的抗性机制研究。IV. C5b-9与血清抗性淋病奈瑟菌而非血清敏感淋病奈瑟菌的细菌外膜成分形成高分子量复合物。
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Killing of gram-negative bacteria by complement. Fractionation of cell membranes after complement C5b-9 deposition on to the surface of Salmonella minnesota Re595.补体对革兰氏阴性菌的杀伤作用。补体C5b-9沉积于明尼苏达沙门氏菌Re595表面后细胞膜的分级分离。
Biochem J. 1989 Oct 15;263(2):505-11. doi: 10.1042/bj2630505.
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Complement attack of altered outer membrane areas synthesized after inhibition of the 3-deoxy-D-manno-octulosonate pathway leads to cell death.在3-脱氧-D-甘露糖辛酸途径受到抑制后合成的改变的外膜区域的补体攻击会导致细胞死亡。
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Studies on the mechanism of bacterial resistance to complement-mediated killing. III. C5b-9 deposits stably on rough and type 7 S. pneumoniae without causing bacterial killing.细菌对补体介导杀伤的抗性机制研究。III. C5b-9稳定沉积于粗糙型和7型肺炎链球菌上,不会导致细菌杀伤。
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Interaction of fluid phase C1/C1q and macrophage membrane-associated C1q with gram-negative bacteria.液相C1/C1q与巨噬细胞膜相关C1q与革兰氏阴性菌的相互作用。
Behring Inst Mitt. 1989 Jul(84):236-54.

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