Su Wenya, Wang Wenjia, Li Ling, Zhang Mengge, Xu Hai, Fu Chengzhang, Pang Xiuhua, Wang Mingyu
State Key Laboratory of Microbial Technology, Microbial Technology Institute, Shandong University, Qingdao 266237, PR China.
Helmholtz Institute for Pharmaceutical Research Saarland (HIPS), Helmholtz Centre for Infection Research (HZI), and Department of Pharmacy, Saarland University, Saarbrücken 66123, Germany.
Eng Microbiol. 2024 Aug 17;4(3):100165. doi: 10.1016/j.engmic.2024.100165. eCollection 2024 Sep.
Tigecycline serves as a critical "final-resort" antibiotic for treating bacterial infections caused by multidrug-resistant bacteria for which treatment options are severely limited. The increasing prevalence of tigecycline resistance, particularly among Gram-negative bacteria, is a major concern. Various mechanisms have been identified as contributors to tigecycline resistance, including upregulation of nonspecific Resistance Nodulation Division (RND) efflux pumps due to mutations in transcriptional regulators, enzymatic modification of tigecycline by monooxygenase enzymes, and mutations affecting tigecycline binding sites. This review aims to consolidate our understanding of tigecycline resistance mechanisms in Gram-negative bacteria and offer insights and perspectives for further drug development.
替加环素是治疗由多重耐药菌引起的细菌感染的关键“最后手段”抗生素，而这类细菌的治疗选择极为有限。替加环素耐药性的日益普遍，尤其是在革兰氏阴性菌中，是一个主要问题。已确定多种机制是替加环素耐药性的成因，包括由于转录调节因子突变导致非特异性耐药结节化分裂（RND）外排泵上调、单加氧酶对替加环素进行酶促修饰以及影响替加环素结合位点的突变。本综述旨在巩固我们对革兰氏阴性菌中替加环素耐药机制的理解，并为进一步的药物研发提供见解和观点。
