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Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes

Áron Dernovics1, György Seprényi2, Zsolt Rázga3

  • 1Department of Medical Microbiology, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 10., H-6720 Szeged, Hungary.

Biomedicines
|November 25, 2023
PubMed
Abstract

Insights

Staphylococcus aureus phenol-soluble modulin alpha3 (PSMα3) stimulates autophagy in skin cells. This increased autophagic activity may be a defense mechanism to maintain skin homeostasis.

Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Phenol-soluble modulins (PSMs) are pore-forming toxins produced by staphylococci.
  • PSMs have diverse cellular effects, including lytic, pro-apoptotic, pro-inflammatory, and antimicrobial actions.
  • The impact of PSMs on autophagy remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of recombinant PSMα3 on autophagic activity in HaCaT keratinocytes.
  • To elucidate the role of PSMα3 in cellular defense mechanisms.

Main Methods:

  • Western blot analysis to assess autophagic flux and marker proteins (LC3B).
  • Indirect immunofluorescence assay for LC3B and Beclin-1 localization.
  • Transmission electron microscopy for ultrastructural analysis.
  • Acridine orange staining for cytoplasmic acidification.
  • Phospho-kinase array and Western blot to study signaling pathways.

Main Results:

  • PSMα3 treatment increased autophagosome formation and acidic vesicular organelles.
  • Elevated LC3B-II levels and stimulated autophagic flux were observed.
  • PSMα3 induced accumulation of autophagosomes, amphisomes, and multilamellar bodies.
  • Decreased phospho-Akt and phospho-mTOR, with increased phospho-Erk1/2 levels.

Conclusions:

  • PSMα3 significantly stimulates autophagy in HaCaT keratinocytes.
  • Enhanced autophagy by PSMα3 may represent a cellular defense mechanism.
  • This process could contribute to maintaining skin homeostasis.
Keywords:
autophagykeratinocytephenol-soluble modulinpore-forming toxinstaphylococci

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