介绍肽聚糖循环及细菌对β-内酰胺类药物的耐药机制,为相关教学和科研工作提供参考。通过查阅文献,结合自身科研工作,对β-内酰胺类抗生素的抑菌机制和细菌对β-内酰胺类抗生素的耐药机制进行综述;β-内酰胺类抗生素可与转肽酶等蛋白质结合,破坏肽聚糖平衡,从而阻碍细胞正常生长;而细菌可通过β-内酰胺酶的诱导、外排泵的表达、外膜通透性增加和靶蛋白的修饰等措施来应对β-内酰胺类抗生素的作用,从而产生耐药。与肽聚糖循环有关的蛋白质,如转肽酶和转糖基酶,可作为β-内酰胺类新抗生素的筛选靶标;与细菌耐药性产生有关的蛋白质,如β-内酰胺酶,可作为β-内酰胺类抗生素辅助药物的筛选靶标。
Abstract
To introduce peptidoglycan recycling and the β-lactams resistance mechanisms of bacteria, so that some help would be supplied to corresponding scientific workers and university teachers. By searching literatures, combined with our own studies, the bactericidal mechanisms of β-lactams and the resistance mechanisms of bacteria to β-lactams were summarized. The bactericidal activity of β-lactams is resulted from the inhibition of cell wall biosynthesis through combination with penicillin binding proteins such as transpeptidase destruction of peptidoglycan balances between biosynthesis and hydrolysis. The drug resistance of bacteria is resulted from the induction of β-lactamase, expression of out-pumping proteins, increase of outmembrane permeability, and modification of antibiotic target proteins. The proteins related to peptidoglycan recycling, such as transpeptidase and glycosyltransferase, would be potential targets for screening new β-lactams. The proteins related to β-lactams resistance, such as β-lactamase, would be potential targets for screening adjuvant drugs of β-lactams.
关键词
细胞壁 /
β-内酰胺类抗生素 /
肽聚糖循环 /
青霉素结合蛋白 /
裂解性糖基转移酶
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Key words
cell wall /
β-lactam /
peptidoglycan cycle /
penicillin binding protein /
lytic transglycosylase
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中图分类号：
R978
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脚注
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基金
浙江省自然科学基金资助项目(LY17C010003);浙江大学微生物学国家精品课程建设经费(20150602)
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