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α-Hemolysin enhances Staphylococcus aureus internalization and survival within mast cells by modulating the

Oliver Goldmann1, Lorena Tuchscherr2, Manfred Rohde3

  • 1Infection Immunology Research Group, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124, Braunschweig, Germany.

Cellular Microbiology
|November 24, 2015
PubMed

Insights

Staphylococcus aureus evades mast cell defenses by upregulating alpha-hemolysin (Hla) to increase bacterial entry. This Hla-ADAM10 interaction boosts beta1 integrin on mast cells, enhancing S. aureus internalization.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Mast cells (MCs) are crucial for host defense against pathogens.
  • Staphylococcus aureus previously shown to evade MC extracellular defenses via internalization.
  • Molecular mechanisms of S. aureus internalization by MCs require elucidation.

Purpose of the Study:

  • Investigate the molecular mechanisms by which S. aureus evades mast cell antimicrobial activities.
  • Elucidate the role of alpha-hemolysin (Hla) and beta1 integrins in S. aureus internalization by MCs.

Main Methods:

  • Analyzed S. aureus gene expression in response to MC antimicrobial mediators.
  • Investigated the interaction between S. aureus Hla and ADAM10 on MCs.
  • Assessed the effect of Hla and Hla-ADAM10 inhibition on bacterial internalization.
  • Quantified beta1 integrin expression on MCs following Hla exposure.

Main Results:

  • S. aureus up-regulates Hla, fibronectin-binding protein A, and regulatory systems upon exposure to MC mediators.
  • S. aureus Hla induces beta1 integrin expression on MCs via Hla-ADAM10 interaction.
  • Deletion of Hla or inhibition of Hla-ADAM10 interaction significantly impairs S. aureus internalization.
  • Purified Hla induces dose-dependent up-regulation of beta1 integrin on MCs.

Conclusions:

  • S. aureus employs a counter-defense strategy against MCs by up-regulating fibronectin-binding proteins and inducing Hla-ADAM10-mediated beta1 integrin expression.
  • This mechanism enhances S. aureus internalization into MCs through fibronectin-binding protein and beta1 integrin interactions.

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