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

肠出血性大肠杆菌（EHEC）越来越被认为是流行病和散发疾病的常见原因，特别是血性腹泻和溶血性尿毒症综合征。疫情爆发的常见来源可以追溯到食用受污染的汉堡包、其他食品和饮用水。从样品中恢复病原菌不容易。然而，这种恢复病原体的失败可能不是因为生物体的缺失，而是因为细胞进入了所谓的可存活但不可培养（VBNC）状态。大肠杆菌O157在低温灭菌的蒸馏水微生物中变得不可培养。我们可以复苏不可培养的细胞，将它们接种到含有过氧化氢酶或丙酮酸钠等非酶过氧化物降解化合物的琼脂培养基上。过氧化氢酶或丙酮酸的作用模式是通过代谢副产物H2O2的降解，而不是通过补充不可培养细胞恢复所需的营养物质。我们的研究基于这样的假设：大肠杆菌O157对饥饿和低温的反应是进入不可培养状态，而在琼脂平板上接种细菌时，氧化应激的纠正可以促进不可培养细胞的恢复。结果表明，大肠杆菌的sigma因子特别是sigma 38在进入VBNC状态中起着重要作用。

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.