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Staphylococcus aureus β-hemolysin causes skin inflammation by acting as an agonist of epidermal growth factor

Yonggen Jia1, Zhangchun Guan2,3, Chenghua Liu2

  • 1Beijing Institute of Tropical Medicine, Beijing Friendship Hospital, Capital Medical University , Beijing, China.

Microbiology Spectrum
|December 7, 2023
PubMed
Abstract

Insights

Staphylococcus aureus skin infections may be worsened by beta-hemolysin (Hlb), a bacterial toxin that activates epidermal growth factor receptor (EGFR). A new monoclonal antibody targeting Hlb offers a potential treatment for these inflammatory skin diseases.

Area of Science:

  • Microbiology
  • Dermatology
  • Immunology

Background:

  • Staphylococcus aureus is a common cause of human skin infections.
  • The molecular mechanisms underlying S. aureus-induced skin pathogenesis are not fully understood.
  • Epidermal Growth Factor Receptor (EGFR) signaling plays a role in skin homeostasis and disease.

Purpose of the Study:

  • To elucidate the molecular pathogenesis of S. aureus skin infections.
  • To identify novel therapeutic targets for S. aureus-related skin conditions.
  • To investigate the role of beta-hemolysin (Hlb) in S. aureus pathogenesis and its interaction with EGFR.

Main Methods:

  • Molecular analysis of S. aureus isolates.
  • In vitro assays to assess Hlb activity and EGFR activation.
  • Development and characterization of a neutralizing monoclonal antibody against Hlb.

Main Results:

  • S. aureus beta-hemolysin (Hlb) acts as an agonist of EGFR.
  • Hlb secreted by S. aureus is a risk factor for EGFR-related skin diseases.
  • A novel monoclonal antibody effectively neutralizes Hlb activity.

Conclusions:

  • Hlb is a key virulence factor in S. aureus skin infections, contributing to pathogenesis via EGFR activation.
  • Targeting Hlb with neutralizing antibodies presents a promising therapeutic strategy for S. aureus-related inflammatory skin diseases.
  • This study deepens the understanding of the link between S. aureus colonization and inflammatory skin conditions.
Keywords:
ADAM17EGFRStaphylococcus aureusskin inflammationsphingomyelinaseβ-hemolysin

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