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Protein F1 and Streptococcus pyogenes resistance to phagocytosis

Kendra A Hyland1, Beinan Wang, P Patrick Cleary

  • 1Department of Microbiology, University of Minnesota Medical School, MMC196, 420 Delaware Street S.E., Minneapolis, MN 55455, USA. hyla0021@umn.edu

Infection and Immunity
|March 21, 2007
PubMed

Insights

Streptococcus pyogenes protein F1 (PrtF1/SfbI) confers resistance to phagocytosis and inhibits complement C3 deposition. This finding suggests PrtF1/SfbI has immune evasion properties similar to M protein in S. pyogenes infections.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Streptococcus pyogenes causes human pharyngitis and possesses fibronectin-binding proteins.
  • M protein and protein F1 (PrtF1/SfbI) are differentially regulated and mediate epithelial cell invasion.
  • The study investigates shared properties between PrtF1/SfbI and M protein.

Purpose of the Study:

  • To determine if PrtF1/SfbI exhibits additional functional similarities to M protein.
  • To assess the role of PrtF1/SfbI in S. pyogenes' interaction with the host immune system.

Main Methods:

  • Utilized an M-negative Streptococcus pyogenes mutant.
  • Expressed PrtF1/SfbI in the M-negative mutant.
  • Assessed resistance to phagocytosis.
  • Measured C3 deposition on the bacterial surface.

Main Results:

  • Expression of PrtF1/SfbI in an M-negative mutant conferred resistance to phagocytosis.
  • PrtF1/SfbI expression resulted in partial inhibition of C3 deposition.
  • These effects suggest immune evasion capabilities of PrtF1/SfbI.

Conclusions:

  • PrtF1/SfbI shares immune evasion properties with M protein.
  • PrtF1/SfbI contributes to Streptococcus pyogenes' survival against host defenses.
  • Further research into PrtF1/SfbI function is warranted for understanding pathogenesis.

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