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耐亚胺培南铜绿假单胞菌中不可渗透性与染色体β-内酰胺酶活性的相互作用

Interplay of impermeability and chromosomal beta-lactamase activity in imipenem-resistant Pseudomonas aeruginosa.

作者信息

Livermore D M

机构信息

Department of Medical Microbiology, London Hospital Medical College, United Kingdom.

出版信息

Antimicrob Agents Chemother. 1992 Sep;36(9):2046-8. doi: 10.1128/AAC.36.9.2046.

Abstract

Mutational loss of the D2 porin causes imipenem resistance in Pseudomonas aeruginosa. It was found that this mechanism could function only when the chromosomal beta-lactamase was expressed. Mutants lacking both the beta-lactamase and the D2 porin were almost as susceptible as those that lacked the beta-lactamase but retained the porin. Thus, imipenem resistance reflected an interplay of the enzyme and impermeability, not either factor alone. These findings suggest that the activity of a carbapenem more beta-lactamase stable than imipenem should be less affected by the porin loss. Meropenem approached this behavior.

摘要

D2孔蛋白的突变性缺失导致铜绿假单胞菌对亚胺培南耐药。研究发现,这种机制只有在染色体β-内酰胺酶表达时才起作用。同时缺乏β-内酰胺酶和D2孔蛋白的突变体与缺乏β-内酰胺酶但保留孔蛋白的突变体几乎一样敏感。因此,亚胺培南耐药反映了酶和通透性的相互作用,而非单一因素所致。这些发现表明,一种比亚胺培南对β-内酰胺酶更稳定的碳青霉烯类药物的活性受孔蛋白缺失的影响应较小。美罗培南接近这种特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9ab/192435/4588cde7350f/aac00043-0278-a.jpg

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