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Published on: February 7, 2013
Alcohol increases hemolysis by staphylococci
Moshe Korem1, Yael Gov, Natali Shirron
1Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Alcohol enhances the hemolytic activity of staphylococci, including Staphylococcus aureus and Staphylococcus epidermidis. This effect involves the upregulation of virulence regulator RNAIII and altered hemolysin production, suggesting new mechanisms of bacterial virulence.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
Background:
- Alcohols have recently been shown to induce hemolytic properties in certain yeasts.
- Staphylococci are Gram-positive bacteria known for their pathogenic potential, often mediated by hemolysins.
Purpose of the Study:
- To investigate the phenomenon of alcohol-enhanced hemolysis in various staphylococcal species.
- To elucidate the molecular mechanisms underlying alcohol-induced hemolysis in Staphylococcus aureus and Staphylococcus epidermidis.
Main Methods:
- Comparative analysis of hemolytic activity in different strains of Staphylococcus aureus and Staphylococcus epidermidis in the presence of ethanol and n-butanol.
- Quantitative assessment of virulence regulator RNAIII expression and hemolysin production (alpha, beta, gamma) using molecular techniques.
- Examination of specific mutant strains (S. aureus 8325-4 DeltaTRAP, RN6911) to identify RNAIII-independent mechanisms.
Main Results:
- Ethanol and n-butanol significantly upregulated RNAIII and increased alpha, beta, and gamma-hemolysin production in S. aureus strain 8325-4.
- In S. aureus strains COL and SH1000, RNAIII increased but hemolysin transcription levels remained unchanged.
- Staphylococcus epidermidis strain sofi showed increased RNAIII and beta-hemolysin production.
- S. aureus mutant strains exhibited no changes in RNAIII or hemolysin transcription, suggesting alternative hemolytic pathways.
Conclusions:
- Alcohol can promote hemolysis in staphylococci through RNAIII-dependent and potentially RNAIII-independent mechanisms.
- Further research is needed to identify other hemolysins or mechanisms (e.g., hyperoxidation, cytotoxic lipids) responsible for alcohol-enhanced hemolysis in certain strains.
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