Influence of RecA on in vivo virulence and Shiga toxin 2 production in Escherichia coli pathogens
Influence of RecA on in vivo virulence and Shiga toxin 2 production in Escherichia coli pathogens
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DOI：
10.1006/mpat.1999.0279
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发表时间：
1999-07-01
影响因子：
3.8
通讯作者：
Hacker, J
中科院分区：
文献类型：
--
作者：
Fuchs, S;Mühldorfer, I;Hacker, J
将肠出血性大肠埃希菌（EHEC） O157:H7 933株、86-24株和尿路致病性大肠埃希菌（UPEC） 536株与其等基因recA突变株和recA反式补充株进行小鼠静脉致死性和肺毒性试验。虽然野生型肠出血性大肠杆菌菌株具有完全的毒力，但recA突变株的毒力却大大降低。将肠出血性大肠杆菌recA突变体与克隆的大肠杆菌recA基因互补，恢复了它们的毒力。stx(2) EHEC突变体TUV86-2及其等基因突变体recA在两种检测中都是完全无毒的。RecA对UPEC菌株536的毒力没有影响。我们得出结论，肠出血性大肠杆菌的致死率可能主要是由于志贺毒素，由于缺乏自发噬菌体诱导，志贺毒素在recA突变体中严重下调。因此，我们比较了肠出血性大肠杆菌recA（+）菌株933和86-24与recA（-）菌株产生志贺毒素2 （Stx2）的情况。肠出血性大肠杆菌菌株的recA突变体毒素合成明显减少，并且不产生Stx2特异性噬菌体。将肠出血性大肠杆菌recA突变体与克隆的recA基因互补，使recA突变体能够恢复毒素和噬菌体的产生。这些结果表明，EHEC菌株中较高水平的Stx2合成是由RecA控制的较高水平的Stx2特异性噬菌体自发诱导的结果。(C) 1999学术出版社。
The enterohemorrhagic Escherichia coli (EHEC) O157:H7 strains 933 and 86-24 as well as the uropathogenic E. coli (UPEC) strain 536 were compared with their isogenic recA mutants and recA trans-complemented strains in intravenous lethality and lung toxicity assays in mice. While the wild-type EHEC strains were fully virulent, the virulence of the recA mutants was strongly reduced. Complementation of the EHEC recA mutants with the cloned E. coli recA gene restored their virulence capacity. The stx(2) EHEC mutant TUV86-2 as well as its isogenic recA mutant were completely avirulent in both assays. In contrast, RecA had no influence on the virulence of UPEC strain 536. We conclude that the lethality observed with EHEC is presumably mainly due to Shiga toxin, which is severely down-regulated in the recA mutants as a result of lacking spontaneous phage induction. Therefore, the EHEC recA(+) strains 933 and 86-24 were compared for their Shiga toxin 2 (Stx2) production with the respective recA(-) counterparts. The recA mutants of the EHEC strains were significantly reduced in toxin synthesis and were devoid of Stx2 specific phage production. Complementation of the EHEC recA mutants with the cloned recA gene enabled the recA mutants to restore toxin and phage production. These results suggest that the higher level of Stx2 synthesis in the EHEC strains is the result of a higher level of spontaneous Stx2 specific phage induction, which is controlled by RecA. (C) 1999 Academic Press.