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Cytotoxic effect of hemolytic culture supernatant from Enterococcus faecalis on mouse polymorphonuclear neutrophils

S Miyazaki1, A Ohno, I Kobayashi

  • 1Department of Microbiology, Toho University School of Medicine, Tokyo, Japan.

Insights

Hemolytic Enterococcus faecalis strains are more lethal than nonhemolytic strains. Their hemolysin targets specific erythrocyte lipids, like phosphatidylcholine, and also damages immune cells, impacting virulence.

Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Enterococcus faecalis is an opportunistic pathogen.
  • Hemolytic strains of E. faecalis exhibit increased virulence.
  • The specific mechanisms of E. faecalis hemolysin activity are not fully understood.

Purpose of the Study:

  • To reconfirm the lower LD50 of hemolytic E. faecalis strains.
  • To investigate the erythrocyte membrane components involved in hemolysin-mediated lysis.
  • To determine the effect of hemolytic E. faecalis supernatant on immune cells.

Main Methods:

  • LD50 determination in normal mice.
  • Erythrocyte lysis assays using erythrocytes from various species.
  • Lipid inhibition assays with sphingomyelin and phosphatidylcholine.
  • Cytotoxicity assays with mouse polymorphonuclear neutrophils and macrophages.

Main Results:

  • Hemolytic E. faecalis strains had significantly lower LD50s than nonhemolytic strains.
  • E. faecalis hemolysin lysed erythrocytes from humans, horses, rabbits, and mice, but not cows or sheep.
  • Phosphatidylcholine, present in susceptible erythrocytes, inhibited hemolysin-induced lysis.
  • Hemolytic culture supernatant also lysed mouse polymorphonuclear neutrophils and macrophages.

Conclusions:

  • Hemolytic E. faecalis exhibits enhanced virulence, correlating with lower LD50 values.
  • Phosphatidylcholine is identified as a likely binding component for E. faecalis hemolysin on erythrocyte membranes.
  • E. faecalis hemolysin possesses cytotoxic effects not only on erythrocytes but also on key immune cells, suggesting a broader role in pathogenesis.

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