Insights into the Mechanism of Action of Bactericidal Lipophosphonoxins

PLoS One. 2015 Dec 30;10(12):e0145918. doi: 10.1371/journal.pone.0145918. eCollection 2015.

Abstract

The advantages offered by established antibiotics in the treatment of infectious diseases are endangered due to the increase in the number of antibiotic-resistant bacterial strains. This leads to a need for new antibacterial compounds. Recently, we discovered a series of compounds termed lipophosphonoxins (LPPOs) that exhibit selective cytotoxicity towards Gram-positive bacteria that include pathogens and resistant strains. For further development of these compounds, it was necessary to identify the mechanism of their action and characterize their interaction with eukaryotic cells/organisms in more detail. Here, we show that at their bactericidal concentrations LPPOs localize to the plasmatic membrane in bacteria but not in eukaryotes. In an in vitro system we demonstrate that LPPOs create pores in the membrane. This provides an explanation of their action in vivo where they cause serious damage of the cellular membrane, efflux of the cytosol, and cell disintegration. Further, we show that (i) LPPOs are not genotoxic as determined by the Ames test, (ii) do not cross a monolayer of Caco-2 cells, suggesting they are unable of transepithelial transport, (iii) are well tolerated by living mice when administered orally but not peritoneally, and (iv) are stable at low pH, indicating they could survive the acidic environment in the stomach. Finally, using one of the most potent LPPOs, we attempted and failed to select resistant strains against this compound while we were able to readily select resistant strains against a known antibiotic, rifampicin. In summary, LPPOs represent a new class of compounds with a potential for development as antibacterial agents for topical applications and perhaps also for treatment of gastrointestinal infections.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Bacterial Agents / chemistry
  • Anti-Bacterial Agents / pharmacokinetics
  • Anti-Bacterial Agents / pharmacology*
  • Bacillus subtilis / drug effects
  • Bacillus subtilis / growth & development
  • Bacillus subtilis / metabolism
  • Biological Transport, Active
  • Caco-2 Cells
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Cell Membrane Permeability / drug effects
  • Drug Discovery
  • Drug Stability
  • Enterococcus faecalis / drug effects
  • Enterococcus faecalis / growth & development
  • Female
  • Gram-Positive Bacteria / drug effects
  • Gram-Positive Bacteria / metabolism
  • Humans
  • Male
  • Mice
  • Mice, Inbred ICR
  • Microbial Sensitivity Tests
  • Microscopy, Electron, Transmission
  • Molecular Structure
  • Protein Binding
  • Pyrimidine Nucleosides / chemistry
  • Pyrimidine Nucleosides / pharmacokinetics
  • Pyrimidine Nucleosides / pharmacology*
  • Streptococcus agalactiae / drug effects
  • Streptococcus agalactiae / growth & development

Substances

  • Anti-Bacterial Agents
  • Pyrimidine Nucleosides

Grants and funding

This work was supported by Technological Agency of the Czech Republic, www.tacr.cz, TA02010035 DR; Czech Science Foundation, www.gacr.cz, P305/12/G034 LK; Czech Science Foundation, www.gacr.cz, 13-18051P GS. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The funder TRIOS Ltd provided support in the form of salaries for authors [TL], but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific role of this author is articulated in the ‘author contributions’ section.