Mai Zifeng, Li Jiahui, Zhan Zeqiang, Tian Xiaorong, Hou Wanwan, He Mu, Shi Chunlei
State Key Laboratory of Microbial Metabolism, Department of Food Science & Technology, School of Agriculture & Biology, Shanghai Jiao Tong University, Shanghai 200240, China.
Foods. 2025 Jul 22;14(15):2566. doi: 10.3390/foods14152566.
, a major cause of foodborne illness globally, presents significant challenges due to its multidrug resistance and biofilm-forming capabilities. Pyruvate carboxylase (PycA), a metabolic master switch linking glycolysis and the tricarboxylic acid (TCA) cycle, is a potential target for controlling . In this study, a mutant was constructed and analyzed using phenotypic assays and proteomics to investigate its role in virulence and antimicrobial resistance. The results showed that deletion of in the foodborne methicillin-resistant strain ATCC BAA1717 resulted in a 4- to 1024-fold reduction in resistance to β-lactams, aminoglycosides, and macrolides; a 23.24% impairment in biofilm formation; and a 22.32% decrease in staphyloxanthin production, a key antioxidant essential for survival in oxidative food environments. Proteomic analysis revealed downregulation of the TCA cycle, purine biosynthesis, surface adhesins (FnbA/B, SasG), and β-lactamase (BlaZ), linking PycA-mediated metabolism to phenotypes relevant to food safety. These findings underscore the importance of PycA as a metabolic regulator crucial for resilience in food systems, suggesting novel strategies to combat foodborne staphylococcal infections through metabolic interference.
作为全球食源性疾病的主要病因，因其多重耐药性和生物膜形成能力而带来重大挑战。丙酮酸羧化酶（PycA）是连接糖酵解和三羧酸（TCA）循环的代谢主开关，是控制[原文此处缺失具体细菌名称]的潜在靶点。在本研究中，构建了一个[原文此处缺失具体基因名称]突变体，并通过表型分析和蛋白质组学进行分析，以研究其在毒力和抗菌耐药性中的作用。结果表明，在食源性耐甲氧西林菌株ATCC BAA1717中缺失[原文此处缺失具体基因名称]导致对β-内酰胺类、氨基糖苷类和大环内酯类药物的耐药性降低4至1024倍；生物膜形成能力受损23.24%；金黄色葡萄球菌黄素（一种在氧化性食品环境中生存所必需的关键抗氧化剂）产量下降22.32%。蛋白质组学分析显示TCA循环、嘌呤生物合成、表面黏附素（FnbA/B、SasG）和β-内酰胺酶（BlaZ）下调，将PycA介导的代谢与食品安全相关表型联系起来。这些发现强调了PycA作为一种代谢调节因子对于食品系统中[原文此处缺失具体细菌名称]恢复力的重要性，提示了通过代谢干扰对抗食源性葡萄球菌感染的新策略。
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