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Staphylococcus aureus Virulent PSMα Peptides Induce Keratinocyte Alarmin Release to Orchestrate IL-17-Dependent Skin

Seitaro Nakagawa1, Masanori Matsumoto2, Yuki Katayama1

  • 1Department of Dermatology, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.

Cell Host & Microbe
|November 10, 2017
PubMed

Insights

Staphylococcus aureus virulence peptides, phenol-soluble modulin alpha (PSMα), trigger skin inflammation. Keratinocyte signaling via Myd88, IL-1R, and IL-36R drives an IL-17-mediated response to S. aureus skin infection.

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Staphylococcus aureus colonization of the epidermis is common, but host sensing mechanisms for virulent strains remain unclear.
  • Understanding how the skin distinguishes between commensal and virulent S. aureus is crucial for inflammatory response research.

Purpose of the Study:

  • To elucidate the mechanisms by which the host senses virulent Staphylococcus aureus on the skin.
  • To identify the specific bacterial factors and host signaling pathways involved in S. aureus-induced cutaneous inflammation.

Main Methods:

  • Utilized a murine epicutaneous infection model.
  • Investigated the role of phenol-soluble modulin alpha (PSMα) in triggering inflammation.
  • Analyzed the involvement of keratinocyte-derived IL-1α and IL-36α, and their receptors (IL-1R, IL-36R).
  • Assessed the function of the signaling adaptor Myd88 in keratinocytes and systemically.
  • Examined IL-17 production by γδ T cells and ILC3, and neutrophil infiltration.
  • Utilized Il17a-/-f-/- mice to evaluate the role of IL-17 in inflammation.

Main Results:

  • S. aureus-expressed PSMα is essential for inducing cutaneous inflammation.
  • PSMα triggers the release of keratinocyte IL-1α and IL-36α.
  • Signaling through IL-1R and IL-36R is required for IL-17 induction.
  • Myd88 deletion in keratinocytes or systemically significantly reduced inflammatory markers and immune cell infiltration.
  • Mice lacking IL-17 showed blunted inflammatory responses to S. aureus.

Conclusions:

  • Keratinocyte Myd88 signaling, activated by S. aureus PSMα, is a key driver of IL-17-mediated skin inflammation.
  • This pathway is critical for mounting an appropriate immune response to epicutaneous S. aureus infection.
Keywords:
Agr virulenceIL-1IL-36Myd88PSMsS. aureusalarminspathogen virulenceskin infection

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