Trimethoprim resistance in Pseudomonas aeruginosa is instigated by genetic mutations in the prtN gene
Antibiotic-resistant Pseudomonas aeruginosa(PAO1)poses a significant challenge in clinical infec-tions,highlighting the importance of studying its resistance mechanisms for improving clinical treatments.Our study found that the △prtN 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 in △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 pyo-cin biosynthesis gene and prtN exhibited slightly reduced Tmp resistance.In contrast,the lipopolysaccharide-deficient strain △wbpL showed slightly increased Tmp resistance.In △prtN,the expression levels of reactive ox-ygen species(ROS)-related genes(oxyR,katA,ahpC),biofilm formation,and antibiotic resistance associat-ed with efflux pumps showed no significant difference compared to the wild type.In conclusion,the Tmp resist-ance observed in the prtN mutant is likely due to the regulatory effects of PrtN on S-type pyocins and lipopo-lysaccharide-related targets.
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