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Enterococcus faecalis suppresses Staphylococcus aureus-induced NETosis and promotes bacterial survival in

Patrick Hsien-Neng Kao1,2, Jun-Hong Ch'ng3,4,5,6, Kelvin K L Chong2

  • 1School of Biological Sciences, Nanyang Technological University, Singapore 637551.

FEMS Microbes
|October 30, 2023
PubMed

Insights

Enterococcus faecalis suppresses neutrophil extracellular trap formation (NETosis) during polymicrobial infections, promoting Staphylococcus aureus survival. This immune evasion highlights complex host responses in wound infections.

Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis

Background:

  • Enterococcus faecalis is an opportunistic pathogen often found with other microbes in wound infections.
  • E. faecalis can enhance co-infecting microbe survival through interbacterial synergy and immune subversion.
  • The impact of E. faecalis-mediated immune suppression on co-infecting microbes is not well understood.

Purpose of the Study:

  • To investigate if E. faecalis attenuates neutrophil-mediated responses in mixed-species infections.
  • To determine the effect of E. faecalis on neutrophil extracellular trap formation (NETosis) during Staphylococcus aureus co-infection.
  • To elucidate the mechanisms by which E. faecalis influences the host immune response in polymicrobial infections.

Main Methods:

  • Investigated neutrophil responses to E. faecalis and Staphylococcus aureus in co-infection models.
  • Assessed phagocytosis, reactive oxygen species (ROS) production, degranulation, and NETosis.
  • Analyzed the effect of E. faecalis on histone citrullination during S. aureus-induced NETosis.

Main Results:

  • Neutrophils control E. faecalis via phagocytosis, ROS production, and degranulation but not NETosis.
  • E. faecalis actively suppresses S. aureus-induced NETosis by interfering with histone citrullination.
  • E. faecalis evades NET-associated killing mechanisms, correlating with increased S. aureus survival.

Conclusions:

  • E. faecalis actively suppresses neutrophil extracellular trap formation (NETosis) in polymicrobial infections.
  • This suppression of NETosis by E. faecalis promotes the survival of co-infecting bacteria like S. aureus.
  • Attenuated pathogen-specific immune responses contribute to the pathogenesis of polymicrobial wound infections.
Keywords:
Enterococcus faecalisStaphylococcus aureusneutrophil extracellular trapsneutrophilspolymicrobial infection

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