School of Cellular and Molecular Medicine, University of Bristol Biomedical Sciences Building, University Walk, Bristol BS8 1TD, United Kingdom.
School of Cellular and Molecular Medicine, University of Bristol Biomedical Sciences Building, University Walk, Bristol BS8 1TD, United Kingdom.
J Mol Biol. 2019 Aug 23;431(18):3472-3500. doi: 10.1016/j.jmb.2019.04.002. Epub 2019 Apr 5.
The β-lactams retain a central place in the antibacterial armamentarium. In Gram-negative bacteria, β-lactamase enzymes that hydrolyze the amide bond of the four-membered β-lactam ring are the primary resistance mechanism, with multiple enzymes disseminating on mobile genetic elements across opportunistic pathogens such as Enterobacteriaceae (e.g., Escherichia coli) and non-fermenting organisms (e.g., Pseudomonas aeruginosa). β-Lactamases divide into four classes; the active-site serine β-lactamases (classes A, C and D) and the zinc-dependent or metallo-β-lactamases (MBLs; class B). Here we review recent advances in mechanistic understanding of each class, focusing upon how growing numbers of crystal structures, in particular for β-lactam complexes, and methods such as neutron diffraction and molecular simulations, have improved understanding of the biochemistry of β-lactam breakdown. A second focus is β-lactamase interactions with carbapenems, as carbapenem-resistant bacteria are of grave clinical concern and carbapenem-hydrolyzing enzymes such as KPC (class A) NDM (class B) and OXA-48 (class D) are proliferating worldwide. An overview is provided of the changing landscape of β-lactamase inhibitors, exemplified by the introduction to the clinic of combinations of β-lactams with diazabicyclooctanone and cyclic boronate serine β-lactamase inhibitors, and of progress and strategies toward clinically useful MBL inhibitors. Despite the long history of β-lactamase research, we contend that issues including continuing unresolved questions around mechanism; opportunities afforded by new technologies such as serial femtosecond crystallography; the need for new inhibitors, particularly for MBLs; the likely impact of new β-lactam:inhibitor combinations and the continuing clinical importance of β-lactams mean that this remains a rewarding research area.
β-内酰胺类抗生素在抗菌药物中占有重要地位。在革兰氏阴性菌中,水解四元β-内酰胺环酰胺键的β-内酰胺酶是主要的耐药机制,多种酶通过移动遗传元件在机会致病菌(如肠杆菌科(如大肠杆菌)和非发酵菌(如铜绿假单胞菌))中传播。β-内酰胺酶分为四类;活性部位丝氨酸β-内酰胺酶(A、C 和 D 类)和锌依赖性或金属β-内酰胺酶(MBLs;B 类)。本文综述了对每种酶类的机制理解的最新进展,重点介绍了越来越多的晶体结构(特别是β-内酰胺复合物的晶体结构)以及中子衍射和分子模拟等方法如何提高对β-内酰胺分解的生物化学的理解。第二个重点是β-内酰胺酶与碳青霉烯类抗生素的相互作用,因为耐碳青霉烯类细菌是严重的临床关注问题,并且碳青霉烯类水解酶(如 A 类的 KPC、B 类的 NDM 和 D 类的 OXA-48)在全球范围内广泛传播。本文概述了β-内酰胺酶抑制剂的不断变化的格局,以β-内酰胺类抗生素与二氮杂双环辛烷酮和环状硼酸丝氨酸β-内酰胺酶抑制剂的组合在临床上的应用为例,并介绍了在临床上有用的 MBL 抑制剂方面的进展和策略。尽管β-内酰胺酶的研究历史悠久,但我们认为,包括围绕机制的持续未解决的问题;新技术(如连续飞秒晶体学)带来的机会;对新抑制剂的需求,特别是对 MBL 的需求;新的β-内酰胺:抑制剂组合的可能影响以及β-内酰胺类抗生素的持续临床重要性,这意味着这仍然是一个有价值的研究领域。