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A bacterial antibiotic-resistance gene that complements the human multidrug-resistance P-glycoprotein gene

H W van Veen1, R Callaghan, L Soceneantu

  • 1Department of Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Haren, The Netherlands. h.w.van.veen@biol.rug.nl

Nature
|January 24, 1998
PubMed

Insights

Bacterial antibiotic resistance protein LmrA functions like human P-glycoprotein. Expressing LmrA in human cells conferred multidrug resistance, showing conserved drug efflux pump mechanisms from bacteria to humans.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Microbiology

Background:

  • Bacteria develop antibiotic resistance through various mechanisms.
  • Lactococcus lactis protein LmrA extrudes compounds, conferring antibiotic resistance.
  • LmrA is an ATP-binding cassette (ABC) transporter, unlike other bacterial multidrug-resistance proteins.

Purpose of the Study:

  • To investigate the function and characteristics of bacterial LmrA in human cells.
  • To compare LmrA's drug resistance mechanisms with human P-glycoprotein.
  • To explore the conservation of multidrug-resistance efflux pumps across species.

Main Methods:

  • Expressed bacterial lmrA gene in human lung fibroblast cells.
  • Assessed drug resistance phenotypes in engineered human cells.
  • Compared pharmacological properties and drug-binding sites of LmrA and human P-glycoprotein.

Main Results:

  • LmrA localized to the plasma membrane of human cells and conferred multidrug resistance.
  • LmrA and P-glycoprotein showed similar affinities for vinblastine and magnesium-ATP.
  • Inhibitors of P-glycoprotein also blocked LmrA-mediated drug resistance.
  • Kinetic analysis revealed two allosterically linked drug-binding sites in LmrA, identical to P-glycoprotein.

Conclusions:

  • Bacterial LmrA and human P-glycoprotein are functionally interchangeable.
  • The multidrug-resistance efflux pump mechanism is conserved from bacteria to humans.
  • Findings suggest potential strategies for reversing antibiotic resistance in pathogens.

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