Hao Jing-Yi, Lei Yu-Qing, Shi Jun-Yan, Zhao Wan-Bin, Gan Zhi-Lin, Hu Xin, Sun Ai-Dong
College of Biological Sciences and Biotechnology, Beijing Forestry University, Beijing 100083, China.
Beijing Key Laboratory of Forest Food Processing and Safety, Beijing 100083, China.
Foods. 2022 Aug 8;11(15):2377. doi: 10.3390/foods11152377.
The application of high hydrostatic pressure (HHP) technology in the food industry has generated potential safety hazards due to sub-lethally injured (SI) pathogenic bacteria in food products. To address these problems, this study explored the repair mechanisms of HHP-induced SI O157:H7. First, the repair state of SI O157:H7 (400 MPa for 5 min) was identified, which was cultured for 2 h (37 °C) in a tryptose soya broth culture medium. We found that the intracellular protein content, adenosine triphosphate (ATP) content, and enzyme activities (superoxide dismutase, catalase, and ATPase) increased, and the morphology was repaired. The transcriptome was analyzed to investigate the molecular mechanisms of SI repair. Using cluster analysis, we identified 437 genes enriched in profile 1 (first down-regulated and then tending to be stable) and 731 genes in profile 2 (up-regulated after an initial down-regulation). KEGG analysis revealed that genes involved in cell membrane biosynthesis, oxidative phosphorylation, ribosome, and aminoacyl-tRNA biosynthesis pathways were enriched in profile 2, whereas cell-wall biosynthesis was enriched in profile 1. These findings provide insights into the repair process of SI O157:H7 induced by HHP.
由于食品中存在经高静水压(HHP)亚致死损伤的致病细菌,HHP技术在食品工业中的应用产生了潜在的安全隐患。为解决这些问题,本研究探索了HHP诱导的O157:H7亚致死损伤的修复机制。首先,确定了O157:H7亚致死损伤(400 MPa处理5分钟)的修复状态,将其在胰蛋白胨大豆肉汤培养基中于37°C培养2小时。我们发现细胞内蛋白质含量、三磷酸腺苷(ATP)含量以及酶活性(超氧化物歧化酶、过氧化氢酶和ATP酶)增加,且形态得到修复。通过分析转录组来研究亚致死损伤修复的分子机制。利用聚类分析,我们鉴定出在模式1(先下调然后趋于稳定)中富集的437个基因和在模式2(初始下调后上调)中富集的731个基因。KEGG分析表明,参与细胞膜生物合成、氧化磷酸化、核糖体和氨酰-tRNA生物合成途径的基因在模式2中富集,而细胞壁生物合成在模式1中富集。这些发现为HHP诱导的O157:H7亚致死损伤修复过程提供了见解。