铜绿假单胞菌<italic style="font-style: italic">prtN</italic>突变引起甲氧苄啶耐药

肖悦; 王冲; 司玉洁; 韩雪; 段康民; 陈林

doi:10.16152/j.cnki.xdxbzr.2024-05-013

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铜绿假单胞菌prtN突变引起甲氧苄啶耐药

西北大学生物学科办学100周年专刊 | 更新时间：2024-09-30

- 铜绿假单胞菌prtN突变引起甲氧苄啶耐药
- Trimethoprim resistance in Pseudomonas aeruginosa is instigated by genetic mutations in the prtN gene
- 西北大学学报（自然科学版） 2024年54卷第5期页码：909-918
- 作者机构：
  
  西北大学　生命科学学院/西部资源生物与现代生物技术教育部重点实验室，陕西　西安　710069
- 作者简介：
  
  肖悦，女，从事微生物相关研究，xiaoyue_xy2@163.com。
  陈林，男，博士，讲师，从事微生物基因功能、应用微生物等相关研究，chenlin@nwu.edu.cn。
- 基金信息：
  
  陕西省自然科学基金(2019JM-372)
- DOI：10.16152/j.cnki.xdxbzr.2024-05-013
  中图分类号： R378
- 纸质出版日期：2024-10-25，
  
  收稿日期：2024-08-10，
- 稿件说明：
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肖悦, 王冲, 司玉洁, 等. 铜绿假单胞菌prtN突变引起甲氧苄啶耐药[J]. 西北大学学报（自然科学版）, 2024,54(5):909-918.

XIAO Yue, WANG Chong, SI Yujie, et al. Trimethoprim resistance in Pseudomonas aeruginosa is instigated by genetic mutations in the prtN gene[J]. Journal of Northwest University (Natural Science Edition), 2024,54(5):909-918.
肖悦, 王冲, 司玉洁, 等. 铜绿假单胞菌prtN突变引起甲氧苄啶耐药[J]. 西北大学学报（自然科学版）, 2024,54(5):909-918. DOI： 10.16152/j.cnki.xdxbzr.2024-05-013.

XIAO Yue, WANG Chong, SI Yujie, et al. Trimethoprim resistance in Pseudomonas aeruginosa is instigated by genetic mutations in the prtN gene[J]. Journal of Northwest University (Natural Science Edition), 2024,54(5):909-918. DOI： 10.16152/j.cnki.xdxbzr.2024-05-013.

摘要

耐药铜绿假单胞菌（PAO1）在临床感染过程中造成非常棘手的问题，研究其耐药机制有助于临床的治疗。研究结果表明，相对于野生型，Δ

prtN

表现出明显的甲氧苄啶（Tmp）抗性。为了了解其抗性出现的机理，测定了Tmp作用靶点

folA

的表达情况。相比于PAO1

folA

在Δ

prtN

中的表达并未升高，反而有所下降。进一步研究发现，PrtN调控的S型绿脓杆菌素基因和

prtN

的双突变体对Tmp的抗性稍有降低，而脂多糖缺陷菌株Δ

wbpL

对Tmp的抗性略有升高。在Δ

prtN

中活性氧（ROS）相关基因（

oxyR

，

katA

，

ahpC

）的表达水平、生物被膜及外排泵相关抗生素抗性检测结果都显示与野生型无显著性差异。综上，

prtN

基因突变引起的Tmp抗性可能是通过PrtN调控S型绿脓杆菌素及脂多糖相关靶标作用的结果。

Abstract

Antibiotic-resistant

Pseudomonas aeruginosa

(PAO1) poses a significant challenge in clinical infections

highlighting the importance of studying its resistance mechanisms for improving clinical treatments. Our study found that the Δ

prtN

exhibited significant resistance to tr

imethoprim (Tmp) compared to the wild type. To elucidate the underlying mechanism of this resistance

we assessed the expression of

folA

the target of Tmp. Interestingly

folA

expression in Δ

prtN

was not elevated

instead but rather decreased compared to the PAO1 strain. Further investigations revealed that a double mutant lacking both the PrtN-regulated S type pyocin biosynthesis gene and

prtN

exhibited slightly reduced Tmp resistance. In contrast

the lipopolysaccharide-deficient strain Δ

wbpL

showed slightly increased Tmp resistance. In Δ

prtN

the expression levels of reactive oxygen species(ROS)-related genes (

oxyR

katA

ahpC

)

biofilm formation

and antibiotic resistance associated with efflux pumps showed no significant difference compared to the wild type. In conclusion

the Tmp resistance observed in the

prtN

mutant is likely due to the regulatory effects of PrtN on S-type pyocins and lipopolysaccharide-related targets.

关键词

绿脓杆菌素prtN甲氧苄啶脂多糖ROS

Keywords

pyocinprtNtrimethoprimLPSROS

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铜绿假单胞菌prtN突变引起甲氧苄啶耐药

Trimethoprim resistance in Pseudomonas aeruginosa is instigated by genetic mutations in the prtN gene

DOI：10.16152/j.cnki.xdxbzr.2024-05-013

摘要

Abstract

关键词

Keywords

references