Salmonella Enteritidis is a major cause of foodborne gastroenteritis and is thus a persistent threat to global public health. The acid adaptation response helps Salmonella survive exposure to gastric environment during ingestion. In a previous study we highlighted the damage caused to cell membrane and the regulation of intracellular reactive oxygen species (ROS) in S. Enteritidis. In this study, we applied both physiologic and iTRAQ analyses to explore the regulatory mechanism of acid resistance in Salmonella.

It was found that after S. Enteritidis was subject to a 1 h period of acid adaptation at pH 5.5, an additional 1 h period of acid shock stress at pH 3.0 caused less Salmonella cell death than in non-acid adapted Salmonella cells. Although there were no significant differences between adapted and non-adapted cells in terms of cell membrane damage (e.g., membrane permeability or lipid peroxidation) after 30 min, intracellular ROS level in acid adapted cells was dramatically reduced compared to that in non-acid adapted cells, indicating that acid adaption promoted less ROS generation or increased the ability of ROS scavenging with little reduction in the integrity of the cell membrane. These findings were confirmed via an iTRAQ analysis. The adapted cells were shown to trigger incorporation of exogenous long-chain fatty acids into the cellular membrane, resulting in a different membrane lipid profile and promoting survival rate under acid stress. S. Enteritidis experiences oxidative damage and iron deficiency under acid stress, but after acid adaption S. Enteritidis cells were able to balance their concentrations of intracellular ROS. Specifically, SodAB consumed the free protons responsible for forming reactive oxygen intermediates (ROIs) and KatE protected cells from the toxic effects of ROIs. Additionally, acid-labile proteins released free unbound iron promoting ferroptotic metabolism, and NADH reduced GSSH to G-SH, protecting cells from acid/oxidative stress.

肠炎沙门氏菌是食源性胃肠炎的主要原因，因此对全球公共健康构成持续威胁。酸适应反应可帮助沙门氏菌在摄入期间幸免于胃环境暴露。在先前的研究中，我们强调了对S细胞膜的破坏和细胞内活性氧（ROS）的调节。肠炎。在这项研究中，我们应用了生理和iTRAQ分析来探索沙门氏菌的抗酸调节机制。

发现在S之后。肠炎沙门氏菌在pH 5.5时要经历1小时的酸适应期，在pH 3.0的酸休克压力下再过1小时，与非酸适应性沙门氏菌相比，沙门氏菌细胞死亡要少细胞。尽管适应和未适应的细胞在30分钟后在细胞膜损伤（例如膜通透性或脂质过氧化）方面没有显着差异，但与未适应酸的细胞相比，适应于酸的细胞的细胞内ROS水平显着降低细胞，表明酸适应促进较少的ROS生成或增加ROS清除能力，而细胞膜的完整性几乎没有降低。这些发现通过iTRAQ分析得到了证实。适应细胞显示触发外源长链脂肪酸掺入细胞膜，导致不同的膜脂质概况和提高酸性压力下的存活率。小号。肠炎的经验氧化损伤和酸胁迫下缺铁，但酸适应后小号。肠炎细胞能够平衡细胞内ROS的浓度。具体而言，SodAB消耗了负责形成活性氧中间体（ROIs）的游离质子，并保护了KatE保护的细胞免受ROIs的毒性影响。此外，酸不稳定的蛋白质释放出游离的未结合铁，促进铁素体代谢，而NADH将GSSH还原为G-SH，从而保护细胞免受酸/氧化应激。