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The Sbi Protein Contributes to Staphylococcus aureus Inflammatory Response during Systemic Infection

Cintia Daniela Gonzalez1, Camila Ledo2, Constanza Giai1

  • 1Instituto de Investigaciones en Microbiología y Parasitología Médica (IMPaM), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.

Plos One
|July 1, 2015
PubMed

Insights

Staphylococcal binding immunoglobulin protein (Sbi) is a novel virulence factor in Staphylococcus aureus infections. Sbi promotes inflammation by activating TNFR1 and EGFR signaling, leading to increased IL-6 and neutrophil recruitment.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Staphylococcus aureus is a significant human pathogen causing severe infections.
  • Protein A (SpA) and Staphylococcal binding immunoglobulin protein (Sbi) are key virulence factors that bind IgG Fc, hindering opsonophagocytosis.
  • SpA interacts with TNF-α receptor (TNFR) 1, inducing pro-inflammatory cytokines.

Purpose of the Study:

  • To investigate the role of Sbi in the inflammatory response during Staphylococcus aureus infections.
  • To determine if Sbi, similar to SpA, interacts with TNFR1 and influences inflammatory signaling pathways.

Main Methods:

  • Investigated Sbi's role in inflammation using an in vivo model of staphylococcal infection.
  • Analyzed Sbi-mediated signaling pathways, including TNFR1, EGFR, and MAPKs.
  • Quantified the production of pro-inflammatory cytokines (IL-6) and chemokines (CXCL-1).
  • Assessed neutrophil recruitment to the infection site.

Main Results:

  • Sbi was identified as a novel factor inducing inflammatory responses in staphylococcal infections.
  • Sbi mediates inflammation via TNFR1 and EGFR signaling pathways, activating downstream MAPKs.
  • Sbi expression significantly increased IL-6 production and modulated CXCL-1 expression.
  • Sbi enhanced neutrophil recruitment to the site of infection in vivo.

Conclusions:

  • Sbi is a pro-inflammatory staphylococcal antigen contributing to infection pathogenesis.
  • Sbi's interaction with TNFR1 and EGFR signaling pathways is crucial for its inflammatory effects.
  • Targeting Sbi may offer a therapeutic strategy to mitigate Staphylococcus aureus-induced inflammation.

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