Acierno Carlo, Barletta Fannia, Nevola Riccardo, Rinaldi Luca, Sasso Ferdinando Carlo, Adinolfi Luigi Elio, Caturano Alfredo
Department of Infectious Diseases, San Carlo Hospital, 85100 Potenza, Italy.
Department of Anesthesiology and Intensive Care, San Carlo Hospital, 85100 Potenza, Italy.
Int J Mol Sci. 2025 Jun 11;26(12):5574. doi: 10.3390/ijms26125574.
Antibiotic pressure exerts profound effects on bacterial physiology, not limited to classical genetic resistance mechanisms. Increasing evidence highlights the ability of pathogens to undergo metabolic rewiring-an adaptive, reversible reorganization of core metabolic pathways that promotes survival under antimicrobial stress. This review provides a comprehensive analysis of antibiotic-induced metabolic adaptations, encompassing glycolysis, the tricarboxylic acid cycle, fermentation, redox balance, amino acid catabolism, and membrane biosynthesis. We critically examine how diverse antibiotic classes-including β-lactams, aminoglycosides, quinolones, glycopeptides, polymyxins, and antimetabolites-interact with bacterial metabolism to induce tolerance and persistence, often preceding stable resistance mutations. In parallel, we explore the ecological and host-derived signals-such as immunometabolites and quorum sensing-that modulate these metabolic responses. Therapeutically, targeting metabolic pathways offers promising strategies to potentiate antibiotic efficacy, including enzyme inhibition, metabolic adjuvants, and precision-guided therapy based on pathogen metabolic profiling. By framing metabolic plasticity as a dynamic and evolutionarily relevant phenomenon, this review proposes a unifying model linking transient tolerance to stable resistance. Integrating metabolic rewiring into antimicrobial research, clinical diagnostics, and therapeutic design represents a necessary paradigm shift in combating bacterial persistence and resistance.
抗生素压力对细菌生理学产生深远影响,不仅限于经典的遗传抗性机制。越来越多的证据表明,病原体有能力进行代谢重排——核心代谢途径的一种适应性、可逆性重组,以促进在抗菌应激下的存活。本综述全面分析了抗生素诱导的代谢适应性,包括糖酵解、三羧酸循环、发酵、氧化还原平衡、氨基酸分解代谢和膜生物合成。我们批判性地研究了包括β-内酰胺类、氨基糖苷类、喹诺酮类、糖肽类、多粘菌素类和抗代谢物在内的多种抗生素类别如何与细菌代谢相互作用,从而在稳定的抗性突变之前诱导耐受性和持续性。同时,我们探讨了调节这些代谢反应的生态和宿主衍生信号,如免疫代谢物和群体感应。在治疗方面,靶向代谢途径提供了增强抗生素疗效的有前景的策略,包括酶抑制、代谢佐剂以及基于病原体代谢谱的精准导向治疗。通过将代谢可塑性构建为一种动态且与进化相关的现象,本综述提出了一个将短暂耐受性与稳定抗性联系起来的统一模型。将代谢重排纳入抗菌研究、临床诊断和治疗设计,代表了对抗细菌持续性和抗性的必要范式转变。