Staphylococcal (phospho)lipases promote biofilm formation and host cell invasion

Minh Thu Nguyen, Arif Luqman, Katharina Bitschar, Tobias Hertlein, Johannes Dick, Knut Ohlsen, Barbara Bröker, Birgit Schittek, Friedrich Götz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)


Most Staphylococcus aureus strains secrete two lipases SAL1 and SAL2 encoded by gehA and gehB. These two lipases differ with respect to their substrate specificity. Staphylococcus hyicus secretes another lipase, SHL, which is in contrast to S. aureus lipases Ca 2+ -dependent and has a broad-spectrum lipase and phospholipase activity. The aim of this study was to investigate the role of staphylococcal (phospho) lipases in virulence. For this we constructed a gehA-gehB double deletion mutant in S. aureus USA300 and expressed SHL in agr-positive (accessory gene regulator) and agr-negative S. aureus strains. The lipases themselves have no hemolytic or cytotoxic activity. However, in agr-negative strains SHL-expression caused an upregulation of hemolytic activity. We further show that SHL-expression significantly enhanced biofilm formation probably due to an increase of extracellular DNA release. SHL-expression also increased host cell invasion 4–6-fold. Trioleate, a main triacylglycerol component of mammalian skin, induced lipase production. Finally, in the mouse sepsis and skin colonization models the lipase producing and mutant strain showed no significant difference compared to the WT strain. In conclusion, we show that staphylococcal lipases promote biofilm formation and host cell invasion and thereby contribute to S. aureus virulence.

Original languageEnglish
Pages (from-to)653-663
Number of pages11
JournalInternational Journal of Medical Microbiology
Issue number6
Publication statusPublished - Aug 2018


  • Biofilm
  • Hemolysis
  • Host cell invasion
  • Lipase
  • Staphylococcus
  • Virulence


Dive into the research topics of 'Staphylococcal (phospho)lipases promote biofilm formation and host cell invasion'. Together they form a unique fingerprint.

Cite this