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Metal-mediated modulation of streptococcal cysteine protease activity and its biological implications

Karthickeyan Chella Krishnan1, Santhosh Mukundan2, Julio A Landero Figueroa3

  • 1Department of Molecular Genetics, Biochemistry and Microbiology, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA Department of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota, USA.

Infection and Immunity
|May 7, 2014
PubMed

Insights

Zinc and copper inhibit the activity of streptococcal cysteine protease (SpeB), a key factor in group A Streptococcus (GAS) infections. This metal-mediated inhibition may enhance bacterial virulence and disease severity.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Pathogenesis

Background:

  • Streptococcal cysteine protease (SpeB) is a major virulence factor in group A Streptococcus (GAS) infections.
  • SpeB activity and expression are modulated by bacterial regulatory systems and host factors like iron.
  • Understanding SpeB regulation is crucial for developing strategies against invasive GAS infections.

Purpose of the Study:

  • To investigate the role of iron and other metals in modulating SpeB expression and/or activity.
  • To determine if metal modulation of SpeB can potentiate bacterial virulence.

Main Methods:

  • In vitro assays to assess SpeB activity in the presence of various metals.
  • Bioinformatic analysis using metal-binding site prediction servers to identify potential metal interaction sites in SpeB.
  • Analysis of SpeB's catalytic-dyad residues (Cys47 and His195) in relation to metal binding.

Main Results:

  • Divalent metals zinc and copper were found to inhibit SpeB activity at the posttranslational level.
  • Two putative metal-binding sites in SpeB were identified, with one involving catalytic residues Cys47 and His195.
  • Metal-induced inhibition of SpeB may preserve other essential GAS virulence factors.

Conclusions:

  • Zinc and copper availability can modulate SpeB proteolytic activity.
  • This modulation may enhance bacterial survival and dissemination, potentially exacerbating invasive GAS infections.
  • The findings provide insights into novel mechanisms of GAS virulence regulation.

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