Modification of outer membrane protein profile and evidence suggesting an active drug pump in Enterobacter aerogenes

Stéphane Gayet1, Renaud Chollet, Gérard Molle

  • 1EA2197-IFR 48, Faculté de Médecine, 13385 Marseille Cedex 05. UMR 5048, CNRS, U554 INSERM, 34090 Montpellier, France.

Insights

Multidrug-resistant Enterobacter aerogenes strains exhibit altered outer membrane proteins and O-polysaccharide, suggesting stress-induced resistance mechanisms similar to Escherichia coli.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Drug Resistance

Background:

  • Enterobacter aerogenes is a clinically significant pathogen.
  • Multidrug resistance (MDR) in bacteria poses a major public health threat.
  • Understanding resistance mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying multidrug resistance in two clinical isolates of Enterobacter aerogenes.
  • To characterize the outer membrane protein profiles and O-polysaccharide structures of resistant strains.
  • To explore potential efflux pump involvement in chloramphenicol resistance.

Main Methods:

  • Phenotypic analysis of antibiotic resistance.
  • Outer membrane protein profiling using SDS-PAGE.
  • O-polysaccharide characterization.
  • Analysis of intracellular drug accumulation in the presence of carbonyl cyanide m-chlorophenylhydrazone.

Main Results:

  • Both resistant strains displayed a reduced major porin and overproduced OmpX and LamB outer membrane proteins.
  • A semirough Ra O-polysaccharide phenotype was observed, replacing the full-length O-polysaccharide.
  • One isolate showed increased intracellular chloramphenicol accumulation with an uncoupler, indicating energy-dependent efflux.
  • Resistance strategies resembled those induced by stress in Escherichia coli.

Conclusions:

  • Alterations in outer membrane porins and O-polysaccharide contribute to multidrug resistance in Enterobacter aerogenes.
  • Energy-dependent efflux may play a role in chloramphenicol resistance.
  • The observed resistance mechanisms are analogous to stress responses in Escherichia coli, highlighting conserved bacterial defense strategies.

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