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The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages

Anubha Sagar1, Carolin Klemm, Lara Hartjes

  • 1Institute of Medical Microbiology and Hospital Hygiene, University of Ulm, Ulm, Germany.

Plos One
|April 18, 2013
PubMed

Insights

Group B Streptococcus (GBS) beta-hemolysin impacts bacterial survival. Nonhemolytic GBS mutants survived better in phagocytes, suggesting hemolysin regulation is key for GBS infection.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Streptococcus agalactiae (group B streptococci, GBS) is a significant pathogen causing neonatal infections and invasive disease in vulnerable populations.
  • The GBS β-hemolysin is recognized as a critical virulence factor contributing to invasive GBS infections.

Purpose of the Study:

  • To investigate the role of the S. agalactiae β-hemolysin in the interaction between GBS and professional phagocytes.
  • To determine the influence of β-hemolysin on bacterial survival and host immune responses.

Main Methods:

  • Infection of THP-1 monocytic cells and human granulocytes with wild-type hemolytic S. agalactiae and an isogenic nonhemolytic mutant.
  • Quantification of bacterial survival within phagocytic cells.
  • Measurement of pro-inflammatory cytokine (TNF-α) and chemokine (IL-8) release.

Main Results:

  • Nonhemolytic GBS mutants exhibited significantly higher survival rates in THP-1 cells and granulocytes compared to the wild-type strain.
  • No intracellular bacterial multiplication was observed for either strain.
  • The hemolytic wild-type strain induced significantly greater release of Tumor Necrosis Factor-α (TNF-α) from THP-1 cells than the nonhemolytic mutant, while Interleukin-8 (IL-8) levels were similar.
  • Purified GBS cell wall preparations demonstrated potent pro-inflammatory effects on THP-1 cells.

Conclusions:

  • The S. agalactiae β-hemolysin plays a crucial role in modulating the intracellular survival of the bacteria within host phagocytes.
  • Effective establishment of S. agalactiae in various host niches necessitates tightly regulated expression of the β-hemolysin.

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