Generation and testing of mutants of Enterococcus faecalis in a mouse peritonitis model
Generation and testing of mutants of Enterococcus faecalis in a mouse peritonitis model
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DOI：
10.1086/314453
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发表时间：
1998-11-01
影响因子：
6.4
通讯作者：
Murray, BE
中科院分区：
文献类型：
--
作者：
Singh, KV;Qin, X;Murray, BE
先前描述的小鼠腹膜炎模型用于研究粪肠球菌 OGIRF 菌株的衍生物。添加无菌大鼠粪便提取物 (SRFE) 可使 OGIRF 的 LD50 降低 >10 倍。溶血素的产生导致 LD50 降低 35 倍，并且存活时间短得多，与之前使用不使用 SRFE 的腹膜炎模型得到的结果类似。嘌呤（但不是嘧啶）营养缺陷型的致死率比野生型低得多；明胶酶突变体也被减弱。使用肠球菌选择标记生成自杀载体，以破坏编码粪肠球菌抗原的基因；尽管生长速度较慢，但产生的突变体并未减弱。总之，该模型允许检测减毒突变体，证实了先前关于溶血素是毒力因子的报道，并表明明胶酶在小鼠粪肠球菌毒力中的作用；减毒的嘌呤营养缺陷型可以提供用于开发体内表达系统的载体的系统。
A previously described mouse peritonitis model was used to study derivatives of Enterococcus faecalis strain OGIRF The addition of sterile rat fecal extracts (SRFE) lowered the LD50 of OGIRF >10-fold. Hemolysin production caused a 35-fold lower LD50 and a much shorter survival, similar to previous results using a peritonitis model without SRFE, A purine (but not a pyrimidine) auxotroph was considerably less lethal than wild type; gelatinase mutants were also attenuated. A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gene encoding an E. faecalis antigen; the resulting mutant was not attenuated despite a slower growth rate. In conclusion, this model allows attenuated mutants to be detected, corroborates prior reports that hemolysin is a virulence factor, and suggests a role for gelatinase in virulence of E. faecalis in mice; the attenuated purine auxotroph may provide a system for developing vectors for in vivo expression systems.