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Polyamines inhibit porin-mediated fluoroquinolone uptake in mycobacteria

Jansy Passiflora Sarathy1, Edmund Lee, Véronique Dartois

  • 1Novartis Institute for Tropical Diseases Pte Ltd, Singapore, Singapore. jansy_sarathy@hotmail.com

Plos One
|June 12, 2013
PubMed

Insights

Polyamines, like spermidine, reduce fluoroquinolone uptake in mycobacteria by decreasing outer membrane permeability. This polyamine-induced reduction enhances bacterial survival against fluoroquinolone antibiotics.

Area of Science:

  • Microbiology
  • Pharmacology
  • Biochemistry

Background:

  • Polyamines are known to reduce the permeability of the outer membrane in Escherichia coli, affecting antibiotic uptake.
  • Understanding drug penetration in Mycobacterium species is crucial for developing effective tuberculosis treatments.

Purpose of the Study:

  • To investigate the effect of polyamines on fluoroquinolone uptake in Mycobacterium bovis BCG.
  • To determine the potential of polyamines as adjuncts in combating fluoroquinolone resistance in mycobacteria.

Main Methods:

  • Testing the impact of four polyamines (spermidine, spermine, cadaverine, putrescine) on fluoroquinolone accumulation in M. bovis BCG.
  • Assessing the influence of spermidine on bacterial survival and drug accumulation under varying conditions (dose, pH, replication state).
  • Analyzing gene expression of outer membrane proteins in response to polyamine treatment and replication status.

Main Results:

  • Polyamines significantly reduce fluoroquinolone permeability across the mycobacterial outer membrane.
  • Spermidine exhibited the most potent, reversible, dose-, and pH-dependent inhibition of ciprofloxacin accumulation.
  • Spermidine addition increased M. bovis BCG survival by up to 25-fold after ciprofloxacin exposure.
  • Actively replicating Mycobacterium tuberculosis showed reduced ciprofloxacin uptake with spermidine, unlike non-replicating cultures.
  • Down-regulation of outer membrane proteins was observed during the shift to non-replication.

Conclusions:

  • Polyamines effectively decrease fluoroquinolone uptake in mycobacteria, suggesting a role in modulating outer membrane permeability.
  • Facilitated transport via porin-like proteins is likely involved in mycobacterial fluoroquinolone uptake.
  • Reduced intracellular drug accumulation, particularly in non-replicating states, contributes to phenotypic drug resistance in M. tuberculosis.

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