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,ΔprtN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ΔprtN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ΔwbpL对Tmp的抗性略有升高。在ΔprtN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。
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 theΔprtN exhibited significant resistance to trimethoprim(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 inΔprtN 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 strainΔwbpL showed slightly increased Tmp resistance.InΔprtN,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.
作者
肖悦
王冲
司玉洁
韩雪
段康民
陈林
XIAO Yue;WANG Chong;SI Yujie;HAN Xue;DUAN Kangmin;CHEN Lin(Key Laboratory of Resource Biology and Biotechnology in Western China,Ministry of Education/College of Life Sciences,Northwest University,Xi’an 710069,China)
出处
《西北大学学报（自然科学版）》
CAS
CSCD
北大核心
2024年第5期909-918,共10页
Journal of Northwest University（Natural Science Edition）
基金
陕西省自然科学基金(2019JM-372)。
