Molecular mechanisms related to the entry into viable but nonculturable state of enterohemorrhagic Escherichia coli

肠出血性大肠埃希菌(EHEC)是引起流行性和散发性疾病的常见原因，尤其是血性腹泻和溶血性尿毒症综合征。常见的暴发来源被追溯到食用受污染的汉堡包、其他食物和饮用水。从样品中提取病原体并非易事。然而，这种未能恢复病原体的结果可能不是因为没有有机体，而是因为细胞进入了被称为可存活但不可培养(VBNC)的状态。大肠杆菌O157在低温下在灭菌蒸馏水微观世界中变得不可培养。我们可以复活不可培养的细胞，将它们接种到含有过氧化氢酶或非酶类过氧化氢降解化合物(如丙酮酸钠)的琼脂上。提出的过氧化氢酶或丙酮酸的作用方式是通过降解代谢副产物过氧化氢，而不是通过补充恢复不可培养细胞所需的营养物质。我们的研究是基于这样的假设，即E.ColiO157通过进入非培养状态来对饥饿和低温做出反应，并且在琼脂平板上接种细菌过程中氧化应激的纠正，促进了非培养细胞的恢复。我们还证明了大肠杆菌的西格玛因子，尤其是西格玛38在进入VBNC状态中起着重要的作用。

Enterohemorrhagic Escherichia coli(EHEC) is increasingly recognized as a common cause of both epidemic and sporadic disease, notably bloody diarrhea and hemolytic-uremic syndrome. Common sources of outbreaks have been traced to the consumption of contaminated hamburger, other foods, and drinking water. It was not easy to recover the pathogen from the samples. However, this failure to recover the pathogen may result not because of the absence of the organism, but because the cells entered into what has been termed the viable-but-nonculturable(VBNC) state.Escherichia coli O157 became nonculturable in sterilized distilled water microcosms at low temperature. We could resuscitate the nonculturable cells to inoculate them onto an agar medium amended with catalase or nonenzyme peroxide-degrading compounds such as sodium pyruvate. The proposed mode of action of the catalase or pyruvate is via the degradation of the metabolic by-product H2O2, rather than through supplementation of a required nutrient in the recovery of nonculturable cells. Our studies were based on the assumption that E.coli O157 responds to starvation and a low temperature by entering a nonculturable state and that the correction of oxidative stress during inoculation of bacteria on agar plates, promotes recovery of nonculturable cells. We have also demonstrated that the sigma factor especially sigma 38 of E.coli plays an important role in entering into VBNC state.