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The two-component system ScnRK of Streptococcus mutans affects hydrogen peroxide resistance and murine macrophage

Pei-Min Chen1, Heng-Chang Chen, Chun-Ta Ho

  • 1Department and Graduate Institute of Microbiology, College of Medicine, National Taiwan University, No. 1, Jen Ai Road Section 1, Taipei 10051, Taiwan, ROC.

Microbes and Infection
|March 5, 2008
PubMed

Insights

Streptococcus mutans uses the ScnR/ScnK two-component system (TCS) to evade macrophage killing during infective endocarditis. This system helps bacteria counteract reactive oxygen species (ROS) within macrophages.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Macrophage survival is crucial for virulence in viridians streptococci-induced infective endocarditis (IE).
  • Streptococcus mutans, an opportunistic IE pathogen, exhibits poor survival against phagocytic killing by murine macrophages (RAW 264.7 cells).

Purpose of the Study:

  • To investigate the role of a putative two-component system (TCS), ScnR/ScnK, in Streptococcus mutans' interaction with host macrophages.
  • To elucidate the mechanisms by which S. mutans survives macrophage killing.

Main Methods:

  • Phagocytosis assays using wild-type and scnRK-null mutant strains of S. mutans with RAW 264.7 macrophages.
  • Measurement of reactive oxygen species (ROS) levels within activated macrophages.
  • Assessment of bacterial susceptibility to hydrogen peroxide.

Main Results:

  • scnRK-null mutants showed increased intracellular susceptibility to killing by macrophages compared to wild-type.
  • Wild-type S. mutans significantly reduced ROS levels in macrophages, while scnRK-null mutants did not.
  • Mutants lacking scnR or scnRK were more susceptible to hydrogen peroxide, indicating a role in oxidative stress resistance.
  • scnRK expression was not affected by hydrogen peroxide exposure.

Conclusions:

  • The ScnR/ScnK TCS is essential for Streptococcus mutans to counteract oxidative stress.
  • Inhibition of intracellular ROS formation by the ScnR/ScnK system contributes to S. mutans' resistance to phagocytic killing.
  • This TCS plays a significant role in the pathogenesis of infective endocarditis by enabling bacterial survival within macrophages.

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