Phosphatidylethanolamine Deficiency Impairs Escherichia coli Adhesion by Downregulating Lipopolysaccharide Synthesis, Which is Reversible by High Galactose/Lactose Cultivation

Abstract

As the initiation step of bacterial infection or biofouling, bacterial adhesion on cells or substrates is generally an optimal target for antibacterial design. Phosphatidylethanolamine (PE) is the principal phospholipid in bacteria, and its function in bacterial adhesion remains unclear. In this study, four E. coli strains including two PE-deficient mutants (PE⁻PC⁻ and PE⁻PC⁺strains) and two PE-containing wild-type controls (PE ⁺ PC⁻ strains) were recruited to investigate the influence of PE deficiency on bacterial adhesion. We found that PE deficiency could impair E. coli adhesion on macrophages (human THP-1-derived and mouse RAW264.7 macrophages) or glass coverslips by downregulating lipopolysaccharide (LPS) biosynthesis, which could be reversible by high galactose/lactose but not glucose cultivation. The data imply that PE play important role in bacterial adhesion probably via affecting LPS biosynthesis and suggest that targeting PE biosynthesis is also a potential antibacterial strategy.

Keywords:

• Escherichia coli
• phosphatidylethanolamine
• lipopolysaccharide
• bacterial adhesion
• macrophage
• high sugar cultivation

Acknowledgments

We would like to thank Prof. Xingguo Wang for kindly providing the three E. coli mutants (i.e. AD93, AD93/pDD72, and AD93/ptac67 strains). This study was supported by the National Natural Science Foundation of China (grant #: 81560083) and the Natural Science Foundation of Jiangxi Province (grant #: 20151BAB205005 and 20151BBG70035).

Disclosure statement

The authors report no conflicts of interest.

Additional information

Funding

This study was supported by the National Natural Science Foundation of China (grant #: 81560083) and the Natural Science Foundation of Jiangxi Province (grant #: 20151BAB205005 and 20151BBG70035).