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性和散发性疾病的常见原因，特别是出血性腹泻和溶血性尿毒症综合征。疫情的常见来源可以追溯到食用受污染的汉堡包、其他食物和饮用水。从样品中回收病原体并不容易。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，而是因为细胞进入所谓的活但不可培养（VBNC）状态。大肠杆菌O157在低温下的无菌蒸馏水微宇宙中变得不可培养。我们可以复苏不可培养的细胞，将它们接种到添加过氧化氢酶或非酶过氧化物降解化合物（如丙酮酸钠）的琼脂培养基上。过氧化氢酶或丙酮酸盐的拟议作用模式是通过降解代谢副产物H2O2，而不是通过在不可培养细胞的恢复中补充所需的营养物质。我们的研究是基于这样的假设，即大肠杆菌O157响应饥饿和低温进入一个nonculturable状态，并在琼脂平板上的细菌接种过程中的氧化应激的校正，促进恢复nonculturable细胞。我们还证明了大肠杆菌的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.