Abstract：
Low-moisture foods (LMF) have arisen an increasing concern as vehicles of foodborne pathogens. Cronobacter genus, a class A pathogen in powdered infant formula (PIF), is crucial to the safety of LMF. Researchers have concentrated more on the bacterial survival caused by key hazardous factors, yet they often ignore the alteration of virulence properties in the surviving strains following rehydration of LMF mediated by the key factors. Our previous transcriptional profiling showed that luxS might participate in desiccation response. Herein, we further investigated the role of Cronobacter LuxS under desiccation stress by combining with the phenotypic and gene analysis between the Cronobacter parent and luxS mutant strains. Desiccation stress destructing assays confirmed that luxS can significantly enhance the resistance of Cronobacter towards desiccation. Our results also showed that cell hydrophobicity, aggregation, motility, the content of polysaccharide, and AI-2 synthesis pathway involved in luxS-mediated desiccation response. The luxS mutant strain exhibited higher swimming and swarming motility, more content of capsular polysaccharide, and more rapid of aggregation, but lower hydrophobicity than that of the wild-type strain, whereas desiccation stress would result in a opposite effect on these cell surface properties in ΔluxS during rehydration. Additionally, the comparation of gene expression profiles indicated that low moisture would trigger Cronobacter luxS to promote transport osmoprotectants by regulating the expression of proX, proW, and treC, and suppress the expression of cpsG associated with polysaccharide colanic acid. Notably, this study also discovered for the first time that the luxS-deficiency dramatically attenuated adhesion and invasion to intestinal and brain cells, but ΔluxS subjected to desiccation could aggravate the cell virulence instead. Therefore, thinking the alteration of toxicity caused by low-moisture, approach based on blocking the expression of the luxS gene to prevent Cronobacter in LMF needs to be adopted with caution.
摘要：
低水分食品（LMF）作为食源性病原体的载体引起了越来越多的关注。克隆杆菌属,婴儿配方奶粉（PIF）中的A类病原体，对LMF的安全至关重要。研究人员更多地集中在关键危险因素引起的细菌存活上，然而，它们往往忽略了由关键因素介导的LMF复水后存活菌株毒力特性的改变。我们先前的转录谱分析表明luxS可能参与干燥反应。在这里，我们通过结合Cronobacter亲本和luxS突变株之间的表型和基因分析，进一步研究了CronobacterLuxS在干燥胁迫下的作用。干燥胁迫破坏试验证实，luxS可以显着增强Cronobacter对干燥的抵抗力。我们的研究结果还表明，细胞的疏水性，聚合，运动性,多糖的含量，和AI-2合成途径参与luxS介导的干燥反应。luxS突变株表现出更高的游泳和成群运动，荚膜多糖含量较多，更快速的聚集，但疏水性比野生型菌株低，而干燥应力会在再水合过程中对ΔluxS中的这些细胞表面特性产生相反的影响。此外,基因表达谱的比较表明，低水分会触发Cronobacter通过调节proX的表达来促进转运渗透保护剂，prow,和TreC,并抑制与多糖可乐酸相关的cpsG的表达。值得注意的是,这项研究还首次发现，luxS缺乏症可显着减弱对肠和脑细胞的粘附和侵袭，但是ΔluxS经受干燥反而会加剧细胞毒力。因此,考虑低水分引起的毒性变化，基于阻断luxS基因表达以预防LMF中Cronobacter的方法需要谨慎采用。
