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Staphylococcus aureus-derived virulent phenol-soluble modulin α triggers alarmin release to drive IL-36-dependent

Isana Nakajima1, Ken Fukuda1, Waka Ishida1

  • 1Department of Ophthalmology and Visual Science, Kochi Medical School, Kochi University, Kochi, Japan.

Microbes and Infection
|October 7, 2023
PubMed

Insights

Phenol-soluble modulin alpha (PSMα) from MRSA delays wound healing and causes inflammation in mouse keratitis. This inflammation is driven by the release of IL-36, highlighting PSMα and IL-36 as key factors in Staphylococcus aureus keratitis.

Area of Science:

  • Ophthalmology
  • Microbiology
  • Immunology

Background:

  • Methicillin-resistant Staphylococcus aureus (MRSA) causes keratitis.
  • MRSA produces phenol-soluble modulin alpha (PSMα), but its role in keratitis is unknown.

Purpose of the Study:

  • To investigate the role of PSMα in Staphylococcus aureus keratitis.
  • To determine the inflammatory mechanisms involving PSMα during corneal infection.

Main Methods:

  • Experimental mouse keratitis model.
  • Mouse corneal organ culture.
  • Use of PSMα-producing and PSMα-deficient S. aureus strains.
  • Administration of IL-36 receptor antagonist.

Main Results:

  • PSMα-producing S. aureus delayed epithelial wound healing and induced stromal inflammation in mice.
  • PSMα damaged corneal epithelium and triggered release of IL-1α and IL-36α.
  • IL-36 receptor antagonist reduced keratitis severity, indicating IL-36 dependency.
  • Recombinant PSMα induced IL-36-dependent corneal inflammation.

Conclusions:

  • PSMα is a critical factor in Staphylococcus aureus keratitis pathogenesis.
  • PSMα-induced inflammation is mediated by the IL-36 signaling pathway.
  • Targeting PSMα or IL-36 may offer therapeutic strategies for S. aureus keratitis.
Keywords:
AlarminsInterleukin 36KeratitisPhenol-soluble modulin αStaphylococcus aureusVirulence

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