The FbaB-type fibronectin-binding protein of Streptococcus pyogenes promotes specific invasion into endothelial cells

Silva Amelung1, Andreas Nerlich, Manfred Rohde

  • 1Department of Medical Microbiology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.

Insights

The fibronectin-binding protein FbaB from Streptococcus pyogenes M3 is essential for invading human endothelial cells. This protein triggers a phagocytosis-like uptake, potentially aiding invasive bacterial spread.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Invasive serotype M3 Streptococcus pyogenes frequently cause invasive streptococcal disease.
  • These bacteria can rapidly and efficiently invade primary human endothelial cells (EC).

Purpose of the Study:

  • To identify the specific mechanism and protein responsible for Streptococcus pyogenes M3 invasion of endothelial cells.
  • To characterize the role of the fibronectin-binding protein FbaB in this invasive process.

Main Methods:

  • Utilized heterologous gene expression and allelic replacement techniques.
  • Investigated the uptake mechanism and cellular pathway of FbaB-mediated invasion.
  • Confirmed FbaB's essentiality and sufficiency for endothelial cell invasion.

Main Results:

  • Identified FbaB, a fibronectin-binding protein of M3 S. pyogenes, as a potent endothelial cell (EC) invasin.
  • Demonstrated that FbaB is essential and sufficient to induce EC invasion through a Rac1-dependent, phagocytosis-like mechanism.
  • Showed that FbaB-mediated uptake follows the classical endocytic pathway, leading to lysosomal degradation.

Conclusions:

  • FbaB acts as a novel streptococcal invasin with specific tropism for endothelial cells.
  • FbaB initiates an invasion process that likely contributes to the deep tissue tropism and vascular spread of invasive S. pyogenes.

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