Simulation of mexR of ARP36 by gene editing in CSP18 conferred CSP18 an ARP36-like susceptibility to the aztreonam. The results demonstrated that hyperexpression of an efflux pump MexAB-OprM caused by a R70Q substitution in MexR, contributed to the increased resistance to aztreonam in the isolate ARP36. RNAseq and genomic DNA resequencing were carried out to compare the global transcriptional profiles and in the clinical setting genomic profiles between these two isolates. In this work, we demonstrate a resistance mechanism to aztreonam of a clinical isolate (ARP36) in comparison with a sensitive one (CSP18).
Deciphering the mechanisms of antibiotic resistance development in the clinical setting may provide critical insights into the design of effective combinatory antibiotic therapies to treat P. aeruginosa commonly accumulates genomic mutations which confer them antibiotic resistance and better adaptations to the host environment.
Therapy for Pseudomonas aeruginosa infections is hard due to its high natural and acquirable antibiotic resistance. 2Tianjin Union Medical Center, Nankai University Affiliated Hospital, Tianjin, China.1State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, College of Life Sciences, Nankai University, Tianjin, China.Zhenzhen Ma 1†, Congjuan Xu 1†, Xinxin Zhang 1, Dan Wang 1, Xiaolei Pan 1, Huimin Liu 2, Guangbo Zhu 2, Fang Bai 1, Zhihui Cheng 1, Weihui Wu 1 and Yongxin Jin 1*