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Cytoplasmic replication of Staphylococcus aureus upon phagosomal escape triggered by phenol-soluble modulin α

Magdalena Grosz1, Julia Kolter, Kerstin Paprotka

  • 1Department of Microbiology, University of Würzburg, Biocenter, Am Hubland, D-97074, Würzburg, Germany; Institute for Hygiene and Medical Microbiology, Josef-Schneider-Str. 2, Bldg. E1, D-97080, Würzburg, Germany.

Cellular Microbiology
|October 30, 2013
PubMed

Insights

Staphylococcus aureus uses phenol-soluble $\alpha$ (PSM$\\alpha$) peptides to escape host cell endosomes, enabling intracellular replication. Mutants lacking PSM$\\alpha$ are trapped in phagosomes, preventing bacterial growth within host cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Staphylococcus aureus is a Gram-positive bacterium internalized by various host cells.
  • Intracellular survival of S. aureus may facilitate immune evasion and dissemination.
  • Phenol-soluble modulins (PSMs) are cytolytic peptides, with PSM$\\alpha$ implicated in polymorphonuclear leukocyte killing.

Purpose of the Study:

  • To investigate the role of PSM$\\alpha$ peptides in S. aureus escape from host cell endosomes.
  • To determine if PSM$\\alpha$ is essential for intracellular bacterial replication.
  • To assess the impact of PSM$\\alpha$ on phagosomal integrity.

Main Methods:

  • Comparison of isogenic PSM$\\alpha$ mutants with wild-type S. aureus strains (MRSA and MSSA).
  • Monitoring of intracellular bacterial microenvironment acidity using flow cytometry.
  • Assessment of endosomal integrity via a reporter recruitment technique.

Main Results:

  • PSM$\\alpha$ mutants were impaired in phagosomal escape in both professional and non-professional phagocytes.
  • Mutants in other toxins (PSM$\\beta$, $\\delta$-toxin, $\\beta$-toxin, PI-PLC, PVL) showed wild-type escape efficiencies.
  • Intracellular replication of S. aureus occurred only when the PSM$\\alpha$ operon was functional, indicating cytoplasmic growth after escape.

Conclusions:

  • PSM$\\alpha$ peptides are critical for S. aureus to escape the endosome and enter the host cell cytoplasm.
  • Phagosomal escape mediated by PSM$\\alpha$ is a prerequisite for intracellular replication of S. aureus.
  • Targeting PSM$\\alpha$ may represent a strategy to inhibit intracellular S. aureus infections.

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