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The Mechanism of Antibiotic-tolerance in Adherent bacteria

粘附细菌的抗生素耐受机制

基本信息

批准号：
12671774
负责人：
ONO Tsuneko
金额：
$ 0.64万
依托单位：
The University of Tokushima
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671774/
关键词：
Pseudomonas aeruginosa adherence antibiotics tolerance tcp gene bta gene rpoS gene P. aeruginosa P.pneumoniae ストレス応答熱ショック

项目摘要

In this project, we have studied about the mechanism of antibiotics tolerant in adherent cells of Pseudomonas aeruginosa. The following results were obtained in this study.1. The effect of several types of stress on antibiotic tolerance and the involvement of rpoS gene. It was found that the stationary phase bacteria were more tolerant to antibiotics than log phase bacteria and the rpoS defective mutant was less tolerant than the wild type strain. In early stage after the addition of biapenem, heat shock stress and osmotic stress induced bacterial tolerance to antibiotics. RpoS gene may be involved in the antibiotic tolerance of P. aeruginosa.2. Identification of the genes associating the mechanism of antibiotics tolerant in adherent cells. Transposon Tn1737KH insertion mutants were constructed. One of them, a strain KMX7803, exhibited high tolerance to biapenem, has been obtained. The MBC of biapenem to adherent cells was 8 times higher than that of the wild type. In planktonic cells, the survival of the mutant at 3 hours after the addition of biapenem was about 1000 times higher than that of the wild type.A mutant KMX50, exhibited low tolerance to biapenem, has been obtained. The MIC and MBC of biapenem to strain KMX50 was exactly the same as that of the wild type. In planktonic cells, the survival of the mutant at 2 hours after the addition of biapenem was about 1000 times lower than that of the wild type.In the strain KMX7803, Tn1737KH was inserted in the open reading frame called PA056, which was designated top. In the strain KMX50, the transposon was inserted in the open reading frame called PA2242, which was designated bta.These mutants were useful tools to elucidate the tolerant mechanisms of adherent bacteria to antibiotics.

本课题研究了铜绿假单胞菌贴壁细胞对抗生素的耐受机制。本研究获得了以下结果：1.几种胁迫对抗生素耐药性的影响及rpoS基因的参与。发现稳定期细菌比对数期细菌对抗生素更耐受，并且rpoS缺陷型突变体比野生型菌株耐受性更低。在添加比阿培南后的早期阶段，热休克应激和渗透胁迫诱导细菌对抗生素产生耐受。RpoS基因可能与铜绿假单胞菌的耐药性有关.贴壁细胞耐药相关基因的鉴定。构建转座子Tn1737KH插入突变体。其中一株菌株KMX 7803对比阿培南表现出较高的耐受性。比阿培南对贴壁细胞的MBC是野生型的8倍。在浮游细胞中，添加比阿培南后3小时，突变体的存活率比野生型高约1000倍，获得了一株对比阿培南耐受性较低的突变体KMX 50。比阿培南对KMX 50菌株的MIC和MBC与野生型完全相同。突变株KMX 7803在开放阅读框PA 056中插入Tn1737 KH，命名为top。在KMX 50菌株中，转座子插入到开放阅读框PA 2242中，命名为bta，这些突变体是阐明粘附细菌对抗生素耐受机制的有用工具。