Streptococcus anginosus orchestrates antibacterial potential of NETs facilitating survival of accompanying pathogens

Magdalena Pilarczyk-Zurek1, Joanna Budziaszek1, Keerthanaa Nandagopal1

  • 1Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology of Jagiellonian University, Krakow, Poland.

Microbiological Research
|November 3, 2024
PubMed

Insights

Streptococcus anginosus uses a nuclease, SanA, to disable neutrophil extracellular traps (NETs), aiding its survival in severe infections. This mechanism also protects other bacteria, promoting polymicrobial infections.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Bacterial Pathogenesis

Background:

  • Streptococcus anginosus is an opportunistic pathogen causing severe infections like abscesses and empyema.
  • S. anginosus is frequently found in polymicrobial infections, suggesting interactions with other bacteria.

Purpose of the Study:

  • To investigate the mechanism by which S. anginosus evades the host immune response.
  • To identify virulence factors contributing to S. anginosus pathogenicity in both monospecies and polymicrobial settings.

Main Methods:

  • Analysis of clinical S. anginosus isolates.
  • Characterization of a novel cell wall-anchored nuclease (SanA).
  • Assessment of SanA's role in NET inactivation and bacterial survival assays.

Main Results:

  • S. anginosus actively inactivates neutrophil extracellular traps (NETs).
  • A cell wall-anchored nuclease, SanA, is responsible for NET inactivation.
  • High SanA expression is linked to severe S. anginosus infections.
  • SanA activity protects S. anginosus and coexisting Enterobacteriales from NETs.

Conclusions:

  • SanA is a critical virulence factor for S. anginosus, enabling survival in purulent infections.
  • SanA facilitates polymicrobial infection development by protecting coexisting pathogens.
  • Targeting SanA could be a therapeutic strategy against S. anginosus infections.

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