Wachino Jun-Ichi, Yamaguchi Yoshihiro, Mori Shigetarou, Jin Wanchun, Kimura Kouji, Kurosaki Hiromasa, Arakawa Yoshichika
Department of Bacteriology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Aichi, Japan
Environmental Safety Center, Kumamoto University, Chuo-ku, Kumamoto, Japan.
Antimicrob Agents Chemother. 2016 Jun 20;60(7):4274-82. doi: 10.1128/AAC.03108-15. Print 2016 Jul.
Metallo-β-lactamases (MBLs) confer resistance to carbapenems, and their increasing global prevalence is a growing clinical concern. To elucidate the mechanisms by which these enzymes recognize and hydrolyze carbapenems, we solved 1.4 to 1.6 Å crystal structures of SMB-1 (Serratia metallo-β-lactamase 1), a subclass B3 MBL, bound to hydrolyzed carbapenems (doripenem, meropenem, and imipenem). In these structures, SMB-1 interacts mainly with the carbapenem core structure via elements in the active site, including a zinc ion (Zn-2), Q157[113] (where the position in the SMB-1 sequence is in brackets after the BBL number), S221[175], and T223[177]. There is less contact with the carbapenem R2 side chains, strongly indicating that SMB-1 primarily recognizes the carbapenem core structure. This is the first report describing how a subclass B3 MBL recognizes carbapenems. We also solved the crystal structure of SMB-1 in complex with the approved drugs captopril, an inhibitor of the angiotensin-converting enzyme, and 2-mercaptoethanesulfonate, a chemoprotectant. These drugs are inhibitors of SMB-1 with Ki values of 8.9 and 184 μM, respectively. Like carbapenems, these inhibitors interact with Q157[113] and T223[177] and their thiol groups coordinate the zinc ions in the active site. Taken together, the data indicate that Q157[113], S221[175], T223[177], and the two zinc ions in the active site are key targets in the design of SMB-1 inhibitors with enhanced affinity. The structural data provide a solid foundation for the development of effective inhibitors that would overcome the carbapenem resistance of MBL-producing multidrug-resistant microbes.
金属β-内酰胺酶(MBLs)可使细菌对碳青霉烯类药物产生耐药性,其在全球范围内的日益流行是一个日益严重的临床问题。为了阐明这些酶识别和水解碳青霉烯类药物的机制,我们解析了B3亚类MBL SMB-1(粘质沙雷氏菌金属β-内酰胺酶1)与水解后的碳青霉烯类药物(多利培南、美罗培南和亚胺培南)结合的晶体结构,分辨率为1.4至1.6 Å。在这些结构中,SMB-1主要通过活性位点中的元件与碳青霉烯类药物的核心结构相互作用,这些元件包括一个锌离子(Zn-2)、Q157[113](其中SMB-1序列中的位置在BBL编号后的括号内)、S221[175]和T223[177]。与碳青霉烯类药物R2侧链的接触较少,这强烈表明SMB-1主要识别碳青霉烯类药物的核心结构。这是第一份描述B3亚类MBL如何识别碳青霉烯类药物的报告。我们还解析了SMB-1与已批准药物卡托普利(一种血管紧张素转换酶抑制剂)和2-巯基乙烷磺酸盐(一种化学保护剂)复合物的晶体结构。这些药物是SMB-1的抑制剂,其Ki值分别为8.9和184 μM。与碳青霉烯类药物一样,这些抑制剂与Q157[113]和T223[177]相互作用,并且它们的巯基与活性位点中的锌离子配位。综上所述,数据表明Q157[113]、S221[175]、T223[177]以及活性位点中的两个锌离子是设计具有更高亲和力的SMB-1抑制剂的关键靶点。这些结构数据为开发有效的抑制剂提供了坚实的基础,这些抑制剂将克服产生MBL的多重耐药微生物对碳青霉烯类药物的耐药性。