Asakura Hiroshi, Igimi Shizunobu, Kawamoto Keiko, Yamamoto Shigeki, Makino Sou-Ichi
Division of Biomedical Food Research, National Institute of Health Sciences, Kami-yoga 1-18-1, Setagaya-ku, Tokyo 158-8501, Japan.
FEMS Microbiol Lett. 2005 Dec 15;253(2):243-9. doi: 10.1016/j.femsle.2005.09.039. Epub 2005 Oct 10.
In an enterohemorrhagic Escherichia coli (EHEC) O157:H7 outbreak caused by salted salmon roe that occurred in Japan, 1998, a food isolate (F2) was NaCl-resistant and a patient isolate (P5) was sensitive to NaCl. We show here that hydrogen peroxide, like NaCl, induced a significant loss of culturability in P5. The BacLight assay suggested that the EHEC O157:H7 entered a viable but nonculturable (VNC) state. We used the passage through mice in an attempt to model this transition in phenotype. Mouse-passaged isogenic variants of F2 became NaCl- and oxidation-sensitive, entered the nonculturable state in response to either of these stresses, and could be resuscitated by sodium pyruvate. Since the expression of RpoS in response to these stresses correlated with the isolates' culturabilities, we concluded that in vivo passage negatively modulated RpoS expression, and the subsequent stress exposure induced the VNC state in the EHEC O157:H7 isolates.
在1998年日本因盐渍鲑鱼籽引发的一起肠出血性大肠杆菌（EHEC）O157:H7暴发中，一株食品分离株（F2）对氯化钠具有抗性，而一株患者分离株（P5）对氯化钠敏感。我们在此表明，过氧化氢与氯化钠一样，会导致P5的可培养性显著丧失。BacLight检测表明，EHEC O157:H7进入了活的但不可培养（VNC）状态。我们通过使细菌在小鼠体内传代，试图模拟这种表型转变。经小鼠传代的F2同基因变体对氯化钠和氧化敏感，在受到这些应激中的任何一种时进入不可培养状态，并可被丙酮酸钠复苏。由于RpoS在这些应激下的表达与分离株的可培养性相关，我们得出结论，体内传代对RpoS表达产生负调控，随后的应激暴露诱导EHEC O157:H7分离株进入VNC状态。
