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Phenol-soluble modulin α4 mediates Staphylococcus aureus-associated vascular leakage by stimulating heparin-binding

Lin Li1, Yaya Pian2, Shaolong Chen1

  • 1State Key Laboratory of Pathogen and Biosecurity, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China.

Scientific Reports
|July 8, 2016
PubMed

Insights

Staphylococcus aureus infection causes vascular leakage. We found that the virulence factor phenol-soluble modulin (PSM)α4 triggers heparin-binding protein release from neutrophils, leading to this leakage and potentially offering a therapeutic target.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Vascular leakage is common in severe Staphylococcus aureus infections.
  • The precise mechanisms driving S. aureus-induced vascular leakage are not fully understood.

Purpose of the Study:

  • To elucidate the role of Staphylococcus aureus virulence factors in vascular leakage.
  • To identify specific molecules and pathways involved in S. aureus-induced vascular leakage.

Main Methods:

  • Identified phenol-soluble modulin (PSM)α4 from S. aureus USA300.
  • Investigated PSMα4's effect on heparin-binding protein (HBP) release from polymorphonuclear neutrophils (PMNs).
  • Assessed PSMα4's impact on PMN degranulation, endothelial cell permeability, and in vivo vascular leakage in mice.

Main Results:

  • PSMα4 stimulates HBP release from PMNs, distinct from its cytolytic effects.
  • PSMα4-induced HBP release is mediated by formyl peptide receptor 2 (FPR2) and phosphoinositide 3-kinase (PI3K) signaling.
  • PSMα4 triggers PMN degranulation, increasing myeloperoxidase, elastase release, and CD63 expression.
  • PSMα4-induced HBP release increases endothelial cell permeability in vitro and causes vascular leakage in vivo.

Conclusions:

  • PSMα4 is a novel virulence factor that induces vascular leakage by stimulating HBP release from PMNs.
  • The pathway involves FPR2 and PI3K activation, leading to PMN degranulation.
  • PSMα4 represents a potential therapeutic target for managing S. aureus infections associated with vascular leakage.

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