Wenxi Qi

ORCID: 0009-0008-9886-9893
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About
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Research Areas
  • Antibiotic Resistance in Bacteria
  • Bacterial Genetics and Biotechnology
  • Evolution and Genetic Dynamics
  • Pharmaceutical and Antibiotic Environmental Impacts
  • Cancer therapeutics and mechanisms
  • DNA Repair Mechanisms
  • Virus-based gene therapy research
  • Innovative Microfluidic and Catalytic Techniques Innovation
  • Escherichia coli research studies
  • Microbial infections and disease research
  • CAR-T cell therapy research
  • CRISPR and Genetic Engineering
  • Animal Virus Infections Studies
  • Bacteriophages and microbial interactions
  • Cancer Research and Treatments
  • bioluminescence and chemiluminescence research

University of Amsterdam
2023-2024

Jilin University
2017-2019

Reactive oxygen species (ROS) produced as a secondary effect of bactericidal antibiotics are hypothesized to play role in killing bacteria. If correct, ROS may development de novo resistance. Here we report that single-gene knockout strains with reduced scavenging exhibited enhanced accumulation and more rapid acquisition resistance when exposed sublethal levels antibiotics. Consistent this observation, the scavenger thiourea medium decelerated development. Thiourea downregulated...

10.1016/j.isci.2023.108373 article EN cc-by iScience 2023-11-01

Resistance evolution during exposure to non-lethal levels of antibiotics is influenced by various stress responses bacteria which are known affect growth rate. Here, we aim disentangle how the interplay between resistance development and associated fitness costs affected responses. We performed de novo wild-type strains single-gene knockout in response pathways using four different antibiotics. Throughout development, increase minimum inhibitory concentration (MIC) accompanied a gradual...

10.3390/ijms25052582 article EN International Journal of Molecular Sciences 2024-02-23

Bacteria can acquire resistance through DNA mutations in response to exposure sub-lethal concentrations of antibiotics. According the radical-based theory, reactive oxygen species (ROS), a byproduct respiratory pathway, and oxidative stress caused by metabolic byproducts, play role cell death as secondary killing mechanism. In this study we address question whether ROS also affects development resistance, conditions that cells is not killed antibiotic.To investigate affect de novo...

10.1186/s12866-023-03031-4 article EN cc-by BMC Microbiology 2023-10-02

The stringent response of bacteria to starvation and stress also fulfills a role in addressing the threat antibiotics. Within this response, (p)ppGpp, synthesized by RelA or SpoT, functions as global alarmone. However, effect (p)ppGpp on resistance development is poorly understood. Here, we show that knockout

10.1016/j.isci.2024.109579 article EN cc-by iScience 2024-03-26

Abstract Background : Bacteria can acquire resistance through DNA mutations in response to exposure sub-lethal concentrations of antibiotics. According the radical-based theory, reactive oxygen species (ROS), a byproduct respiratory pathway, and oxidative stress caused by metabolic byproducts, play role cell death as secondary killing mechanism. Results: To investigate whether ROS affect de novo acquisition antibiotic resistance, evolution was compared E. coli wildtype Δ oxyR strains under...

10.21203/rs.3.rs-2932862/v1 preprint EN cc-by Research Square (Research Square) 2023-07-10

Reactive oxygen species (ROS) produced as a secondary effect of bactericidal antibiotics are hypothesized to play role in killing bacteria. If correct, ROS may development de novo resistance. Here we report that single-gene knockout strains with reduced scavenging exhibited enhanced accumulation and more rapid acquisition resistance when exposed sublethal levels antibiotics. Consistent this observation, the scavenger thiourea medium decelerated development. Thiourea downregulated...

10.2139/ssrn.4535253 preprint EN 2023-01-01

Abstract Reactive oxygen species (ROS) produced as a secondary effect of bactericidal antibiotics are hypothesized to play role in killing bacteria. However, the ROS development de novo resistance result sublethal levels has barely been investigated. Here, we report that single-gene knockout strains with reduced scavenging exhibited enhanced accumulation and more rapid acquisition when exposed antibiotics. Consistent this observation, scavenger thiourea medium decelerated development....

10.1101/2023.07.21.550122 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-07-22

Abstract The stringent response of bacteria to starvation and stress, also fulfils a role in addressing the threat antibiotics. Within this response, (p)ppGpp, synthesized by RelA or SpoT, functions as global alarmone. However, effect (p)ppGpp on resistance development is poorly understood. Here, we show that knockout relA rpoS curtails against bactericidal emergence mutations genes such protection factor dps , another synthase spoT Δ -resistant strains, indicates activation responses....

10.21203/rs.3.rs-3404172/v1 preprint EN cc-by Research Square (Research Square) 2023-10-20

Resistance evolution during exposure to non-lethal levels of antibiotics is influenced by various stress responses bacteria which are known affect growth rate. Here, we aim disentangle how the interplay between resistance development and associated fitness costs affected responses. We performed de novo wild-type strains single-gene knockout in response pathways using four different antibiotics. Throughout development, increase minimum inhibitory concentration (MIC) accompanied a gradual...

10.20944/preprints202311.0657.v1 preprint EN 2023-11-09

The stringent response of bacteria to starvation and stress, also fulfils a role in addressing the threat antibiotics. Within this response, (p)ppGpp, synthesized by RelA or SpoT, functions as global alarmone. However, effect (p)ppGpp on resistance development is poorly understood. Here, we show that knockout relA rpoS curtails against bactericidal emergence mutated genes associated with among others, indicates activation responses. growth rate decreased ΔrelA-resistant strains due reduced...

10.2139/ssrn.4706900 preprint EN 2024-01-01
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