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AmpG在介导大肠杆菌丝氨酸β-内酰胺酶诱导与生物膜形成能力之间的动态关系中的作用。

Involvement of AmpG in mediating a dynamic relationship between serine beta-lactamase induction and biofilm-forming ability of Escherichia coli.

作者信息

Mallik Dhriti, Pal Shilpa, Ghosh Anindya S

机构信息

Department of Biotechnology, Indian Institute of Technology Kharagpur, West Bengal-721302, India.

出版信息

FEMS Microbiol Lett. 2018 Apr 1;365(8). doi: 10.1093/femsle/fny065.

Abstract

AmpG permease is implicated both in beta-lactamase induction and peptidoglycan recycling in enterobacterial isolates. Here, physiological studies using molecular genetics show that deletion of AmpG permease dramatically increases beta-lactam susceptibility even in the presence of AmpC, TEM-1 and OXA beta-lactamases. Also, there is an appreciable decrease in the biofilm-forming ability of strains lacking this protein. Expression of this permease in excess probably compromises the integrity of the bacterial cells, leading to cell lysis. Based on these results, we propose that AmpG permease may be used as a potential antibiotic target and its suppression could efficiently inhibit both beta-lactamase induction and biofilm formation.

摘要

AmpG通透酶与肠杆菌属分离株中的β-内酰胺酶诱导和肽聚糖循环均有关联。在此,利用分子遗传学进行的生理学研究表明,即使存在AmpC、TEM-1和OXAβ-内酰胺酶,缺失AmpG通透酶也会显著增加对β-内酰胺的敏感性。此外,缺乏该蛋白的菌株形成生物膜的能力明显下降。过量表达这种通透酶可能会损害细菌细胞的完整性,导致细胞裂解。基于这些结果,我们提出AmpG通透酶可作为潜在的抗生素靶点,抑制该酶可能有效抑制β-内酰胺酶诱导和生物膜形成。

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