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Entry of methotrexate into Streptococcus pneumoniae: a study on a wild-type strain and a methotrexate resistant

Insights

Methotrexate (MTX) enters Streptococcus pneumoniae via a transporter with high affinity for MTX. MTX uptake is energy-dependent and influenced by proton motive force at higher concentrations.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Methotrexate (MTX) is a key chemotherapy drug.
  • Understanding MTX transport in bacteria like Streptococcus pneumoniae is crucial for developing new antimicrobial strategies.
  • The folate pathway is essential for bacterial growth and is a target for MTX.

Purpose of the Study:

  • To investigate the mechanism of methotrexate (MTX) entry into Streptococcus pneumoniae.
  • To determine the role of folate transporters in MTX uptake.
  • To elucidate the energy dependence of MTX transport.

Main Methods:

  • Bacterial growth and uptake assays using radiolabeled MTX.
  • Inhibition studies with folate, folinic acid, and ionophores (CCCP, valinomycin).
  • Experiments with ATP-depleted bacteria to assess energy dependency.
  • Analysis of MTX transport kinetics at various concentrations.

Main Results:

  • MTX uptake in S. pneumoniae showed poor inhibition by folate or folinic acid, suggesting high MTX affinity for its transporter.
  • MTX uptake was non-concentrative and decreased in ATP-depleted bacteria.
  • At high MTX concentrations (1 X 10(-5) M), uptake was linear and energized by the protonmotive force (delta p), indicated by inhibition with ionophores.
  • The high MTX resistance in the amiA9 mutant was not fully explained by reduced MTX uptake.

Conclusions:

  • MTX transport in S. pneumoniae involves a high-affinity transporter, distinct from folate transport.
  • MTX uptake is an active process dependent on cellular energy, likely utilizing the protonmotive force at higher concentrations.
  • Further research is needed to fully understand the mechanisms of MTX resistance in S. pneumoniae.

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