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Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting
Pseudomonas aeruginosa is an important nosocomial pathogen which frequently becomes resistant to most antibiotics used in chemotherapy, resulting in treatment failure among infected individuals. Although the evolutionary trajectory and molecular mechanisms for becoming β-lactam resistant have been w...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9782964/ https://www.ncbi.nlm.nih.gov/pubmed/36557649 http://dx.doi.org/10.3390/microorganisms10122395 |
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author | Liu, Qi Yin, Liwen Zhang, Xinxin Zhu, Guangbo Liu, Huimin Bai, Fang Cheng, Zhihui Wu, Weihui Jin, Yongxin |
author_facet | Liu, Qi Yin, Liwen Zhang, Xinxin Zhu, Guangbo Liu, Huimin Bai, Fang Cheng, Zhihui Wu, Weihui Jin, Yongxin |
author_sort | Liu, Qi |
collection | PubMed |
description | Pseudomonas aeruginosa is an important nosocomial pathogen which frequently becomes resistant to most antibiotics used in chemotherapy, resulting in treatment failure among infected individuals. Although the evolutionary trajectory and molecular mechanisms for becoming β-lactam resistant have been well established for P. aeruginosa, the molecular basis of reversion from β-lactam resistant to susceptible is largely unexplored. In this study, we investigated the molecular mechanisms by which a ceftazidime-resistant clinical strain is converted to a ceftazidime-susceptible isolate under the clinical setting. RNA sequencing and genomic DNA reference mapping were conducted to compare the transcriptional profiles and chromosomal mutations between these two isolates. Our results demonstrate that a gain-of-function mutation in ampD, via deletion of a 53 bp duplicated nucleotide sequence, is the contributory factor for the conversion. Furthermore, we show for the first time that AmpD is involved in intraspecies competitiveness in P. aeruginosa. We also found that AmpD is not responsible for phenotypic changes between R1 and S2, including growth rate, motilities, pyocyanin, rhamnolipid, and biofilm production. This finding provides novel insights into the alteration of β-lactam sensitivity in P. aeruginosa under the clinical setting. |
format | Online Article Text |
id | pubmed-9782964 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-97829642022-12-24 Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting Liu, Qi Yin, Liwen Zhang, Xinxin Zhu, Guangbo Liu, Huimin Bai, Fang Cheng, Zhihui Wu, Weihui Jin, Yongxin Microorganisms Article Pseudomonas aeruginosa is an important nosocomial pathogen which frequently becomes resistant to most antibiotics used in chemotherapy, resulting in treatment failure among infected individuals. Although the evolutionary trajectory and molecular mechanisms for becoming β-lactam resistant have been well established for P. aeruginosa, the molecular basis of reversion from β-lactam resistant to susceptible is largely unexplored. In this study, we investigated the molecular mechanisms by which a ceftazidime-resistant clinical strain is converted to a ceftazidime-susceptible isolate under the clinical setting. RNA sequencing and genomic DNA reference mapping were conducted to compare the transcriptional profiles and chromosomal mutations between these two isolates. Our results demonstrate that a gain-of-function mutation in ampD, via deletion of a 53 bp duplicated nucleotide sequence, is the contributory factor for the conversion. Furthermore, we show for the first time that AmpD is involved in intraspecies competitiveness in P. aeruginosa. We also found that AmpD is not responsible for phenotypic changes between R1 and S2, including growth rate, motilities, pyocyanin, rhamnolipid, and biofilm production. This finding provides novel insights into the alteration of β-lactam sensitivity in P. aeruginosa under the clinical setting. MDPI 2022-12-02 /pmc/articles/PMC9782964/ /pubmed/36557649 http://dx.doi.org/10.3390/microorganisms10122395 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Liu, Qi Yin, Liwen Zhang, Xinxin Zhu, Guangbo Liu, Huimin Bai, Fang Cheng, Zhihui Wu, Weihui Jin, Yongxin Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title | Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title_full | Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title_fullStr | Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title_full_unstemmed | Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title_short | Reversion of Ceftazidime Resistance in Pseudomonas aeruginosa under Clinical Setting |
title_sort | reversion of ceftazidime resistance in pseudomonas aeruginosa under clinical setting |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9782964/ https://www.ncbi.nlm.nih.gov/pubmed/36557649 http://dx.doi.org/10.3390/microorganisms10122395 |
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