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Proteins PblA and PblB of Streptococcus mitis, which promote binding to human platelets, are encoded within a

B A Bensing1, I R Siboo, P M Sullam

  • 1Veterans Affairs Medical Center and the University of California, San Francisco, California 94121, USA.

Infection and Immunity
|September 13, 2001
PubMed

Insights

Bacterial binding to platelets is key in infective endocarditis. Researchers found that Streptococcus mitis proteins PblA and PblB, involved in platelet binding, are encoded by a bacteriophage (SM1), potentially spreading virulence factors.

Area of Science:

  • Microbiology
  • Bacteriology
  • Molecular Biology

Background:

  • Bacterial binding to platelets is a critical factor in infective endocarditis pathogenesis.
  • Surface proteins PblA and PblB from Streptococcus mitis strain SF100 mediate platelet binding.
  • The genes for PblA and PblB are located near genes similar to streptococcal phages, suggesting a prophage origin.

Purpose of the Study:

  • To investigate whether the pblA and pblB genes are located within a prophage in Streptococcus mitis SF100.
  • To determine if these genes are expressed and packaged into phage particles.

Main Methods:

  • Induction of prophage activity using mitomycin C and UV light.
  • Analysis of pblA transcription and PblA/PblB protein expression via quantitative PCR and Western blotting.
  • Identification and characterization of bacteriophage particles using electron microscopy, Southern blotting, and Western blotting.

Main Results:

  • Mitomycin C and UV treatments significantly increased pblA transcription and PblA/PblB protein expression.
  • Electron microscopy revealed phage particles (designated SM1) in induced bacterial cultures.
  • Southern blot confirmed pblA and pblB are within the SM1 genome, and Western blot showed these proteins are present in the phage particles.

Conclusions:

  • The Streptococcus mitis proteins PblA and PblB, involved in platelet binding, are encoded by a lysogenic bacteriophage (SM1).
  • This bacteriophage may serve as a mechanism for disseminating these potential virulence factors among bacterial pathogens.

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