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Isolation and Chemical Characterization of Lipid A from Gram-negative Bacteria
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Isolation and Chemical Characterization of Lipid A from Gram-negative Bacteria

Published on: September 16, 2013

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Phospholipase A1 modulates the cell envelope phospholipid content of Brucella melitensis, contributing to polymyxin

Tobias Kerrinnes1, Briana M Young1, Carlos Leon2

  • 1Department of Medical Microbiology and Immunology, University of California, Davis, Davis, California, USA.

Antimicrobial Agents and Chemotherapy
|August 19, 2015
PubMed

Insights

Brucella melitensis resistance to polymyxin B involves the esterase BveA, which lowers phosphatidylethanolamine (PE) levels. This mechanism is crucial for bacterial survival in macrophages and persistent infections.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Antibiotic Resistance

Background:

  • Polymyxin antibiotics are crucial for treating infections caused by Gram-negative bacteria.
  • High-level polymyxin resistance in bacteria is not fully understood.
  • Brucella species are zoonotic pathogens exhibiting significant resistance to polymyxins.

Purpose of the Study:

  • To investigate novel mechanisms of polymyxin resistance in Brucella melitensis.
  • To identify bacterial factors contributing to high-level resistance against polymyxin B.
  • To elucidate the role of the Brucella melitensis gene bveA in antibiotic resistance and pathogenesis.

Main Methods:

  • Gene knockout of bveA in Brucella melitensis.
  • Biochemical characterization of BveA enzymatic activity.
  • Lipidomic analysis of bacterial membranes.
  • In vitro and in vivo infection models (macrophages, mice).

Main Results:

  • Brucella melitensis gene bveA encodes an esterase with phospholipase A1 activity specific for phosphatidylethanolamine (PE).
  • Loss of bveA leads to increased PE content in bacterial membranes and heightened susceptibility to polymyxin B.
  • BveA is essential for Brucella melitensis survival and replication within macrophages and for establishing persistent infections in mice.
  • BveA homologs are found in alphaproteobacteria coexisting with polymyxin producers, suggesting a conserved strategy.

Conclusions:

  • BveA confers polymyxin B resistance by reducing PE levels in the bacterial cell envelope.
  • BveA is a key virulence factor for Brucella melitensis, impacting host-pathogen interactions.
  • Maintaining low PE content is a potential shared persistence strategy for alphaproteobacteria in diverse host environments.

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