1887

Abstract

Drug efflux pumps transport antimicrobial agents out of bacteria, thereby reducing the intracellular antimicrobial concentration, which is associated with intrinsic and acquired bacterial resistance to these antimicrobials. As genome analysis has advanced, many drug efflux pump genes have been detected in the genomes of bacterial species. In addition to drug resistance, these pumps are involved in various essential physiological functions, such as bacterial adaptation to hostile environments, toxin and metabolite efflux, biofilm formation and quorum sensing. In Gram-negative bacteria, efflux pumps in the resistance–nodulation–division (RND) superfamily play a clinically important role. In this review, we focus on Gram-negative bacteria, including , and , and discuss the role of RND efflux pumps in drug resistance and physiological functions.

Funding
This study was supported by the:
  • Japan Agency for Medical Research and Development
    • Principle Award Recipient: KunihikoNishino
  • Nippon Foundation-Osaka University Project for Infectious Disease Prevention
    • Principle Award Recipient: KunihikoNishino
  • Ministry of Education, Culture, Sports, Science and Technology of Japan
    • Principle Award Recipient: KunihikoNishino
  • Ministry of Education, Culture, Sports, Science and Technology of Japan
    • Principle Award Recipient: SeijiYamasaki
  • Japan Society for the Promotion of Science
    • Principle Award Recipient: KunihikoNishino
  • Japan Society for the Promotion of Science
    • Principle Award Recipient: MitsukoHayashi-Nishino
  • Japan Society for the Promotion of Science
    • Principle Award Recipient: MartijnZwama
  • Japan Society for the Promotion of Science
    • Principle Award Recipient: SeijiYamasaki
  • Takeda Science Foundation
    • Principle Award Recipient: KunihikoNishino
  • Japan Science and Technology Agency (Award CREST)
    • Principle Award Recipient: KunihikoNishino
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.
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2023-06-15
2024-05-04
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