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Phenol-Soluble Modulin Toxins of Staphylococcus haemolyticus
Fei Da1,2, Hwang-Soo Joo1, Gordon Y C Cheung1
1Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of HealthBethesda, MD, United States.
Abstract:
Coagulase-negative staphylococci (CoNS) are important nosocomial pathogens and the leading cause of sepsis. The second most frequently implicated species, after Staphylococcus epidermidis, is Staphylococcus haemolyticus. However, we have a significant lack of knowledge about what causes virulence of S. haemolyticus, as virulence factors of this pathogen have remained virtually unexplored. In contrast to the aggressive pathogen Staphylococcus aureus, toxin production has traditionally not been associated with CoNS. Recent findings have suggested that phenol-soluble modulins (PSMs), amphipathic peptide toxins with broad cytolytic activity, are widespread in staphylococci, but there has been no systematic assessment of PSM production in CoNS other than S. epidermidis. Here, we identified, purified, and characterized PSMs of S. haemolyticus. We found three PSMs of the β-type, which correspond to peptides that before were described to have anti-gonococcal activity. We also detected an α-type PSM that has not previously been described. Furthermore, we confirmed that S. haemolyticus does not produce a δ-toxin, as results from genome sequencing had indicated. All four S. haemolyticus PSMs had strong pro-inflammatory activity, promoting neutrophil chemotaxis. Notably, we identified in particular the novel α-type PSM, S. haemolyticus PSMα, as a potent hemolysin and leukocidin. For the first time, our study describes toxins of this important staphylococcal pathogen with the potential to have a significant impact on virulence during blood infection and sepsis.
Insights
Coagulase-negative staphylococci (CoNS) like Staphylococcus haemolyticus produce phenol-soluble modulins (PSMs). These toxins, including a novel alpha-type PSM, exhibit potent pro-inflammatory and cytolytic activities, contributing to S. haemolyticus virulence in sepsis.
Area of Science:
- Microbiology
- Pathogen Virulence
- Toxinology
Background:
- Coagulase-negative staphylococci (CoNS) are significant nosocomial pathogens, with Staphylococcus haemolyticus being the second most implicated species.
- Knowledge regarding S. haemolyticus virulence factors, particularly toxins, remains limited, contrasting with Staphylococcus aureus.
- Phenol-soluble modulins (PSMs) are amphipathic peptide toxins with broad cytolytic activity, increasingly recognized in staphylococci.
Purpose of the Study:
- To identify, purify, and characterize phenol-soluble modulin (PSM) toxins produced by Staphylococcus haemolyticus.
- To systematically assess PSM production in S. haemolyticus and investigate their functional roles in virulence.
- To explore the potential contribution of these toxins to S. haemolyticus-associated sepsis.
Main Methods:
- Identification and purification of PSMs from S. haemolyticus isolates.
- Characterization of purified PSM peptides, including structural and functional analyses.
- Assessment of the pro-inflammatory and cytolytic activities of identified S. haemolyticus PSMs.
Main Results:
- Three beta-type PSMs and one novel alpha-type PSM (S. haemolyticus PSMα) were identified and characterized in S. haemolyticus.
- S. haemolyticus was confirmed not to produce delta-toxin, aligning with genomic predictions.
- All identified S. haemolyticus PSMs demonstrated significant pro-inflammatory activity, promoting neutrophil chemotaxis.
- The novel S. haemolyticus PSMα was identified as a potent hemolysin and leukocidin.
Conclusions:
- Staphylococcus haemolyticus produces multiple functional phenol-soluble modulins (PSMs), including a novel alpha-type PSM.
- These PSMs possess significant pro-inflammatory and cytolytic activities, contributing to the virulence of S. haemolyticus.
- The identified toxins represent key virulence factors of S. haemolyticus with implications for blood infections and sepsis.
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