Ingestion of Shiga toxin-producing Escherichia coli (STEC) can result in a range of illness severity from asymptomatic to hemorrhagic colitis and death; thus risk assessment of STEC strains for human pathogenicity is important in the area of food safety. Illness severity depends in part on the combination of virulence genes carried in the genome, which can vary between strains even of identical serotype. To better understand how core genes are regulated differently among strains and to identify possible novel STEC virulence gene candidates that could be added to the risk assessment repertoire, we used comparative transcriptomics to investigate global gene expression differences between two STEC strains associated with severe illness and a commensal E. coli strain during in vitro intestinal epithelial cell (IEC) infections. Additionally, we compared a wide array of concomitant cytokine levels produced by the IECs. The cytokine expression levels were examined for a pattern representing STEC pathogenicity; however, while one STEC strain appeared to elicit a proinflammatory response, infection by the other strain produced a pattern comparable to the commensal E. coli. This result may be explained by the significant differences in gene content and expression observed between the STEC strains. RNA-Seq analysis revealed considerable disparity in expression of genes in the arginine and tryptophan biosynthesis/import pathways between the STEC strains and the commensal E. coli strain, highlighting the important role some amino acids play in STEC colonization and survival. Contrasting differential expression patterns were observed for genes involved in respiration among the three strains suggesting that metabolic diversity is a strategy utilized to compete with resident microflora for successful colonization. Similar temporal expression results for known and putative virulence genes were observed in the STEC strains, revealing strategies used for survival prior to and after initial adherence to IECs. Additionally, three genes encoding hypothetical proteins located in mobile genetic elements were, after interrogation of a large set of E. coli genomes, determined to likely represent novel STEC virulence factors.

摄入产生志贺毒素的食物 大肠杆菌（STEC）可能导致多种疾病的严重程度，从无症状到出血性结肠炎甚至死亡；因此，STEC菌株对人类致病性的风险评估在食品安全领域非常重要。疾病的严重程度部分取决于基因组中携带的毒力基因的组合，即使在相同血清型的毒株中，毒力基因的组合也会有所不同。为了更好地了解菌株之间核心基因的调控方式不同，并确定可能添加到风险评估库中的新型STEC毒力候选基因，我们使用了比较转录组学方法，研究了与严重疾病相关的两个STEC菌株之间的总体基因表达差异赞美的大肠杆菌 期间紧张 体外肠上皮细胞（IEC）感染。此外，我们比较了IEC产生的多种伴随细胞因子水平。检查细胞因子表达水平的代表STEC致病性的模式。然而，尽管一个STEC菌株似乎引发了促炎反应，但另一株感染却产生了与普通菌株相当的模式。大肠杆菌。该结果可以通过STEC菌株之间观察到的基因含量和表达的显着差异来解释。RNA-Seq分析显示，精氨酸和色氨酸生物合成/导入途径之间的精氨酸和色氨酸之间的基因表达存在很大差异。大肠杆菌菌株，突显了某些氨基酸在STEC移殖和存活中的重要作用。在三个菌株中观察到与呼吸有关的基因不同的差异表达模式，这表明代谢多样性是一种用于与本地微生物竞争成功定居的策略。在STEC菌株中观察到已知和推定毒力基因的类似时间表达结果，揭示了最初遵循IEC之前和之后用于存活的策略。此外，在对大量的大肠杆菌 确定可能代表新型STEC毒力因子的基因组。