Toxin gene expression by shiga toxin-producing Escherichia coli:: the role of antibiotics and the bacterial SOS response
Toxin gene expression by shiga toxin-producing Escherichia coli:: the role of antibiotics and the bacterial SOS response
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DOI：
10.3201/eid0605.000503
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发表时间：
2000-09-01
影响因子：
11.8
通讯作者：
Barer, MR
中科院分区：
文献类型：
--
作者：
Kimmitt, PT;Harwood, CR;Barer, MR
滋贺毒素产生大肠杆菌（STEC）的毒素合成似乎是通过诱导编码毒素基因的整合噬菌体来协同调节的。噬菌体的产生与细菌SOS反应的诱导有关，SOS反应是一种普遍存在的对DNA损伤的反应。SOS诱导性抗菌剂，特别是喹诺酮类、甲氧苄啶和呋喃唑酮，在其对携带基于染色体的stx 2：：lacZ转录融合的报告STEC菌株的影响的研究中显示诱导毒素基因表达。在高于抑制细菌复制所需的抗菌水平时，这些药物是2型滋贺毒素基因（stx 2）转录的强效诱导剂（高达140倍）;因此，在治疗潜在或确诊的STEC感染患者时应避免使用它们。其他代理商（20研究）和孵育条件产生显着的，但不太引人注目的STX 2转录的影响，积极和消极的影响。SOS介导的毒素合成诱导也提供了一种可能加剧STEC感染和增加sb基因传播的机制。这些特征以及在临床实践和畜牧业中使用SOS诱导抗生素可能是最近出现STEC疾病的原因。
Toxin synthesis by Shiga toxin-producing Escherichia coli (STEC) appears to be coregulated through induction of the integrated bacteriophage that encodes the toxin gene. Phage production is linked to induction of the bacterial SOS response, a ubiquitous response to DNA damage. SOS-inducing antimicrobial agents, particularly the quinolones, trimethoprim, and furazolidone, were shown to induce toxin gene expression in studies of their effects on a reporter STEC strain carrying a chromosome-based stx2::lacZ transcriptional fusion. At antimicrobial levels above those required to inhibit bacterial replication, these agents are potent inducers (up to 140-fold) of the transcription of type 2 Shiga toxin genes (stx2); therefore, they should be avoided in treating patients with potential or confirmed STEC infections. Other agents (20 studied) and incubation conditions produced significant but less striking effects on stx2 transcription; positive and negative influences were observed. SOS-mediated induction of toxin synthesis also provides a mechanism that could exacerbate STEC infections and increase dissemination of sb genes. These features and the use of SOS-inducing antibiotics in clinical practice and animal husbandry may account for the recent emergence of STEC disease.