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.
Abstract:
Streptococcus anginosus is considered an emerging opportunistic pathogen causing life-threatening infections, including abscesses and empyema. Noticeably, clinical data revealed that S. anginosus also constitutes an important component of polymicrobial infections. Here, we showed for the first time that S. anginosus inactivates the antibacterial potential of neutrophil extracellular traps (NETs). The process is determined by a cell wall-anchored nuclease referred to as SanA, which high expression dominates in clinical strains isolated from severe infections. Nuclease activity protects S. anginosus against the antibacterial activity of NETs, supporting at the same time the survival of coexisting highly pathogenic species of Enterobacteriales. Obtained data suggest that SanA nuclease should be recognized as a critical S. anginosus virulence factor determining severe monospecies purulent infections but also shielding other pathogens promoting the development of polymicrobial infections.
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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