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粪肠球菌ATCC 9790的青霉素结合蛋白和青霉素敏感性受生长条件的严重影响:β-内酰胺类抗生素生长抑制间接机制的提议

Streptococcus faecium ATCC 9790 penicillin-binding proteins and penicillin sensitivity are heavily influenced by growth conditions: proposal for an indirect mechanism of growth inhibition by beta-lactams.

作者信息

Fontana R, Canepari P, Satta G, Coyette J

出版信息

J Bacteriol. 1983 May;154(2):916-23. doi: 10.1128/jb.154.2.916-923.1983.

DOI:10.1128/jb.154.2.916-923.1983
PMID:6841320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC217545/
Abstract

The effects of variations in growth conditions on the penicillin response of Streptococcus faecium ATCC 9790 were studied. Changes in the growth temperature and medium composition were found to cause striking changes in the bacterial generation time, cellular penicillin sensitivity (minimum inhibitory concentration), sensitivity of peptidoglycan synthesis to inhibition by penicillin, rate of autolysis, and labeling pattern of penicillin-binding proteins. However, no constant relationship between these parameters and the minimum inhibitory concentration could be observed. Similar electrophoretic patterns for penicillin-binding proteins were observed in cells grown in different media at the optimal growth temperature. Inhibition of cell division by penicillin in cells grown at this temperature (but not at higher or lower temperatures) caused filamentation of the bacteria. In cells grown in a chemically defined medium at the optimal temperature (but not at temperatures above or below), complete inhibition of cell division was associated with only partial inhibition (34% after 150 min) of peptidoglycan synthesis. It is suggested that the status and physiological importance of individual penicillin-binding proteins in S. faecium are heavily influenced by growth conditions. Depending on the growth conditions, different penicillin-binding proteins may perform the cellular function, indispensible for bacterial growth.

摘要

研究了生长条件变化对屎肠球菌ATCC 9790青霉素反应的影响。发现生长温度和培养基成分的变化会导致细菌世代时间、细胞对青霉素的敏感性(最低抑菌浓度)、肽聚糖合成对青霉素抑制的敏感性、自溶速率以及青霉素结合蛋白的标记模式发生显著变化。然而,这些参数与最低抑菌浓度之间未观察到恒定关系。在最佳生长温度下于不同培养基中生长的细胞中观察到相似的青霉素结合蛋白电泳图谱。在此温度(而非更高或更低温度)下生长的细胞中,青霉素对细胞分裂的抑制导致细菌形成丝状体。在最佳温度(而非高于或低于该温度)下于化学限定培养基中生长的细胞中,细胞分裂的完全抑制仅与肽聚糖合成的部分抑制(150分钟后为34%)相关。提示屎肠球菌中各个青霉素结合蛋白的状态和生理重要性受生长条件的严重影响。根据生长条件,不同的青霉素结合蛋白可能执行对细菌生长不可或缺的细胞功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/217545/54a5b8e7e388/jbacter00246-0395-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/217545/815bfa1b7c44/jbacter00246-0393-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/217545/54a5b8e7e388/jbacter00246-0395-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/217545/815bfa1b7c44/jbacter00246-0393-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/217545/54a5b8e7e388/jbacter00246-0395-a.jpg

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1
Streptococcus faecium ATCC 9790 penicillin-binding proteins and penicillin sensitivity are heavily influenced by growth conditions: proposal for an indirect mechanism of growth inhibition by beta-lactams.粪肠球菌ATCC 9790的青霉素结合蛋白和青霉素敏感性受生长条件的严重影响:β-内酰胺类抗生素生长抑制间接机制的提议
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Identification of a streptococcal penicillin-binding protein that reacts very slowly with penicillin.一种与青霉素反应非常缓慢的链球菌青霉素结合蛋白的鉴定。
J Bacteriol. 1983 Sep;155(3):1343-50. doi: 10.1128/jb.155.3.1343-1350.1983.
6
Shifting of the penicillin binding proteins that are the target for inhibition by beta-lactams as a likely mechanism of resistance to antibiotics during therapy.青霉素结合蛋白的改变作为治疗期间对抗生素耐药的一种可能机制,而青霉素结合蛋白是β-内酰胺类药物的抑制靶点。
Chemioterapia. 1985 Feb;4(1):113-5.
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Effects of temperature, NaCl, and methicillin on penicillin-binding proteins, growth, peptidoglycan synthesis, and autolysis in methicillin-resistant Staphylococcus aureus.温度、氯化钠和甲氧西林对耐甲氧西林金黄色葡萄球菌中青霉素结合蛋白、生长、肽聚糖合成及自溶的影响
Antimicrob Agents Chemother. 1987 Nov;31(11):1727-33. doi: 10.1128/AAC.31.11.1727.
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Transition from resistance to hypersusceptibility to beta-lactam antibiotics associated with loss of a low-affinity penicillin-binding protein in a Streptococcus faecium mutant highly resistant to penicillin.在一株对青霉素高度耐药的粪肠球菌突变体中,从对β-内酰胺类抗生素耐药转变为超敏,这与一种低亲和力青霉素结合蛋白的缺失有关。
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引用本文的文献

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Antimicrob Agents Chemother. 1994 Sep;38(9):1980-3. doi: 10.1128/AAC.38.9.1980.
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本文引用的文献

1
The penicillin-binding proteins in Streptococcus faecalis ATCC 9790.粪肠球菌ATCC 9790中的青霉素结合蛋白。
Eur J Biochem. 1980 Sep;110(2):445-56. doi: 10.1111/j.1432-1033.1980.tb04886.x.
2
Identification of the lethal target of benzylpenicillin in Streptococcus faecalis by in vivo penicillin binding studies.通过体内青霉素结合研究鉴定粪肠球菌中苄青霉素的致死靶点。
Nature. 1980 Sep 4;287(5777):70-2. doi: 10.1038/287070a0.
3
Control of cell septation by lateral wall extension in a pH-conditional morphology mutant of Klebsiella pneumoniae.
β-内酰胺类抗生素对大肠杆菌的抑菌和杀菌活性靶点存在于不同的青霉素结合蛋白中。
Antimicrob Agents Chemother. 1995 Apr;39(4):812-8. doi: 10.1128/AAC.39.4.812.
4
Identification of a streptococcal penicillin-binding protein that reacts very slowly with penicillin.一种与青霉素反应非常缓慢的链球菌青霉素结合蛋白的鉴定。
J Bacteriol. 1983 Sep;155(3):1343-50. doi: 10.1128/jb.155.3.1343-1350.1983.
5
Transition from resistance to hypersusceptibility to beta-lactam antibiotics associated with loss of a low-affinity penicillin-binding protein in a Streptococcus faecium mutant highly resistant to penicillin.在一株对青霉素高度耐药的粪肠球菌突变体中,从对β-内酰胺类抗生素耐药转变为超敏,这与一种低亲和力青霉素结合蛋白的缺失有关。
Antimicrob Agents Chemother. 1985 Nov;28(5):678-83. doi: 10.1128/AAC.28.5.678.
6
Regulation of penicillin-binding protein activity: description of a methicillin-inducible penicillin-binding protein in Staphylococcus aureus.青霉素结合蛋白活性的调节:金黄色葡萄球菌中一种甲氧西林诱导型青霉素结合蛋白的描述。
Antimicrob Agents Chemother. 1985 May;27(5):828-31. doi: 10.1128/AAC.27.5.828.
7
Streptococcus faecium mutants that are temperature sensitive for cell growth and show alterations in penicillin-binding proteins.粪肠球菌突变体,对细胞生长温度敏感,且青霉素结合蛋白有改变。
J Bacteriol. 1987 Jun;169(6):2432-9. doi: 10.1128/jb.169.6.2432-2439.1987.
8
Bacteriostatic and bactericidal activities of beta-lactams against Streptococcus (Enterococcus) faecium are associated with saturation of different penicillin-binding proteins.β-内酰胺类药物对粪肠球菌的抑菌和杀菌活性与不同青霉素结合蛋白的饱和有关。
Antimicrob Agents Chemother. 1987 Oct;31(10):1618-26. doi: 10.1128/AAC.31.10.1618.
9
Correlation of penicillin-induced lysis of Enterococcus faecium with saturation of essential penicillin-binding proteins and release of lipoteichoic acid.青霉素诱导的屎肠球菌裂解与必需青霉素结合蛋白的饱和及脂磷壁酸释放的相关性
Antimicrob Agents Chemother. 1990 Oct;34(10):1901-7. doi: 10.1128/AAC.34.10.1901.
10
Mechanisms of resistance of enterococci to beta-lactam antibiotics.肠球菌对β-内酰胺类抗生素的耐药机制。
Eur J Clin Microbiol Infect Dis. 1990 Feb;9(2):103-5. doi: 10.1007/BF01963633.
肺炎克雷伯菌pH条件形态突变体中通过侧壁延伸控制细胞分裂
J Bacteriol. 1980 Apr;142(1):43-51. doi: 10.1128/jb.142.1.43-51.1980.
4
Effects of penicillin on macromolecular synthesis and surface growth of a tolerant streptococcus as studied by computer reconstruction methods.通过计算机重建方法研究青霉素对一株耐受链球菌大分子合成及表面生长的影响。
J Bacteriol. 1980 Dec;144(3):1168-73. doi: 10.1128/jb.144.3.1168-1173.1980.
5
Inhibition of peptidoglycan, ribonucleic acid, and protein synthesis in tolerant strains of Streptococcus mutans.变形链球菌耐受菌株中肽聚糖、核糖核酸和蛋白质合成的抑制作用
Antimicrob Agents Chemother. 1980 Apr;17(4):572-82. doi: 10.1128/AAC.17.4.572.
6
Mechanism of action of penicillins: a proposal based on their structural similarity to acyl-D-alanyl-D-alanine.青霉素的作用机制:基于其与酰基-D-丙氨酰-D-丙氨酸结构相似性的一种假说
Proc Natl Acad Sci U S A. 1965 Oct;54(4):1133-41. doi: 10.1073/pnas.54.4.1133.
7
Penicillin: its basic site of action as an inhibitor of a peptide cross-linking reaction in cell wall mucopeptide synthesis.青霉素:其作为细胞壁粘肽合成中肽交联反应抑制剂的基本作用位点。
Proc Natl Acad Sci U S A. 1965 Jul;54(1):75-81. doi: 10.1073/pnas.54.1.75.
8
Relationship between the latent form and the active form of the autolytic enzyme of Streptococcus faecalis.粪链球菌自溶酶的潜伏形式与活性形式之间的关系。
J Bacteriol. 1969 Nov;100(2):617-24. doi: 10.1128/jb.100.2.617-624.1969.
9
Interaction of penicillin with the bacterial cell: penicillin-binding proteins and penicillin-sensitive enzymes.青霉素与细菌细胞的相互作用:青霉素结合蛋白和青霉素敏感酶。
Bacteriol Rev. 1974 Sep;38(3):291-335. doi: 10.1128/br.38.3.291-335.1974.
10
FL-1060: a new penicillin with a unique mode of action.FL-1060:一种具有独特作用方式的新型青霉素。
Biochem Biophys Res Commun. 1973 Apr 16;51(4):863-8. doi: 10.1016/0006-291x(73)90006-5.