Ferroptosis for food safety: An innovative and sustainable strategy in pathogenic bacteria inactivation and antimicrobial resistance modulation

IF 8.5 1区 生物学 Q1 MICROBIOLOGY
Microbiological research Pub Date : 2026-02-01 Epub Date: 2025-10-08 DOI:10.1016/j.micres.2025.128360
Xinyu Zhou , Jun-Hu Cheng , Xiao Yang , Da-Wen Sun
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引用次数: 0

Abstract

Microbial contamination in food has long posed a significant global public health challenge. The growing antibiotic resistance of foodborne pathogens, particularly multidrug-resistant bacteria, has diminished the effectiveness of traditional antibiotic treatments and increased the public health burden. There is an urgent need for innovative strategies to control foodborne pathogenic bacteria and their resistance. Since the discovery of ferroptosis, a regulatory modality of cell death, researchers have advanced our understanding of its mechanisms. While ferroptosis is primarily observed in eukaryotic cells, some studies indicate that microbial cells also undergo a similar process. This ferroptosis-like death depends on the Fenton reaction and is triggered by iron overload, leading to excessive reactive oxygen species (ROS) and lipid peroxidation. However, current knowledge on ferroptosis-mediated control of foodborne pathogenic bacteria and antimicrobial resistance remains limited. Ferroptosis is primarily triggered by excess intracellular ferrous ions (Fe2+) and disruptions in antioxidant systems. Several studies have utilized this feature to design antimicrobial experiments, which have been successfully applied to antimicrobial infection treatment. Additionally, ferroptosis affects antibiotic-resistant bacteria mainly by inducing direct lethal effects through iron-dependent lipid peroxidation, and disrupting iron homeostasis, which bypasses traditional resistance mechanisms and enhances antibiotic efficacy. This review aims to summarize the concepts, mechanisms, and regulatory measures of ferroptosis while discussing its application in controlling pathogenic bacteria. Further insights into the specific molecular mechanisms of ferroptosis in foodborne pathogenic bacteria are essential to enhance inactivation precision and modulate antimicrobial resistance, thereby facilitating its practical application in food safety.
食品安全:病原菌灭活和抗菌素耐药性调节的创新和可持续战略。
食品中的微生物污染长期以来一直是一个重大的全球公共卫生挑战。食源性病原体,特别是耐多药细菌对抗生素的耐药性日益增强,降低了传统抗生素治疗的有效性,并增加了公共卫生负担。迫切需要创新策略来控制食源性致病菌及其耐药性。自从发现铁下垂,细胞死亡的一种调节方式,研究人员已经提高了我们对其机制的理解。虽然铁下垂主要在真核细胞中观察到,但一些研究表明微生物细胞也经历了类似的过程。这种类似铁中毒的死亡依赖于芬顿反应,由铁超载引发,导致活性氧(ROS)过多和脂质过氧化。然而,目前关于嗜铁中毒介导的食源性致病菌控制和抗菌素耐药性的知识仍然有限。铁死亡主要是由细胞内过量的铁离子(Fe2+)和抗氧化系统的破坏引起的。一些研究利用这一特征设计抗菌实验,并成功应用于抗菌感染治疗。此外,铁中毒对抗生素耐药菌的影响主要是通过铁依赖性脂质过氧化诱导直接致死效应,破坏铁稳态,从而绕过传统的耐药机制,增强抗生素疗效。本文综述了铁下垂的概念、机制和调控措施,并对其在病原菌控制中的应用进行了探讨。进一步了解食源性致病菌中铁死亡的具体分子机制,对于提高其失活精度和调控抗菌素耐药性,从而促进其在食品安全中的实际应用具有重要意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Microbiological research
Microbiological research 生物-微生物学
CiteScore
10.90
自引率
6.00%
发文量
249
审稿时长
29 days
期刊介绍: Microbiological Research is devoted to publishing reports on prokaryotic and eukaryotic microorganisms such as yeasts, fungi, bacteria, archaea, and protozoa. Research on interactions between pathogenic microorganisms and their environment or hosts are also covered.
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