Serrapeptase for Infections? What the Research Says

Key Findings

This in vitro study demonstrated that serrapeptase significantly enhanced the efficacy of vancomycin and rifampicin against both meticillin-resistant (MRSA) and meticillin-susceptible (MSSA) Staphylococcus aureus biofilms. Serrapeptase was identified as one of the two most effective dispersal agents tested (alongside lysostaphin), effectively breaking down the biofilm matrix. The key conclusion is that combining serrapeptase with conventional antibiotics substantially improved biofilm eradication compared to antibiotics alone, suggesting a potential strategy to overcome biofilm-mediated treatment resistance.

Study Design

This was an in vitro observational laboratory study. Researchers assessed the biofilm-dispersing activity of five enzymatic agents (dispersin B, lysostaphin, alpha amylase, V8 protease, serrapeptase) against biofilms formed by 4 clinical MRSA strains and 4 MSSA strains. Biofilms were grown on polystyrene surfaces. Efficacy was measured by quantifying viable bacteria remaining after treatment with enzymes alone or in combination with vancomycin/rifampicin, using standard microbiological plating techniques (colony-forming unit counts). No human or animal subjects were involved; duration pertained to standard biofilm formation and treatment periods in the lab (typically 24-48 hours).

Dosage & Administration

The provided study summary does not specify the exact concentrations or doses of serrapeptase used. Administration was in vitro, meaning serrapeptase was applied directly to the established bacterial biofilms in laboratory culture wells. The method of enzyme delivery (e.g., single dose, continuous exposure) is not detailed in the given abstract.

Results & Efficacy

Serrapeptase significantly enhanced the antibacterial activity of both vancomycin and rifampicin against all 8 S. aureus strains tested (4 MRSA, 4 MSSA). While the abstract states serrapeptase was "one of the most effective dispersal agents," it does not provide specific quantitative reduction percentages or exact p-values for serrapeptase alone. It explicitly states the enhancement of antibiotic efficacy by the dispersal agents was statistically significant (p<0.05 is standard in such microbiological assays, though the exact p-value for serrapeptase combinations isn't quoted in the summary). The key result is the significant reduction in viable biofilm-embedded bacteria when antibiotics were combined with serrapeptase compared to antibiotics alone.

Limitations

Major limitations include the purely in vitro nature of the study, lacking any animal or human data, making direct clinical translation impossible. The specific concentrations of serrapeptase used were not reported in the provided summary, hindering reproducibility assessment. The study only examined short-term biofilm disruption in a controlled lab setting on polystyrene, not on actual medical devices or in complex host environments. It did not investigate potential toxicity of serrapeptase to human cells or in vivo pharmacokinetics. Long-term effects and optimal dosing regimens remain unknown.

Clinical Relevance

This study provides preliminary laboratory evidence that serrapeptase may have a role in disrupting S. aureus biofilms, potentially making antibiotic treatments more effective for stubborn device-related or chronic infections. However, it does not support using serrapeptase supplements to treat infections in humans. The research is foundational, conducted in test tubes, not living organisms. Supplement users should not interpret this as evidence for self-treating bacterial infections with serrapeptase. Its relevance lies in guiding future research into novel anti-biofilm therapies; clinical application would require extensive in vivo and human trials to establish safety, effective dosing, and delivery methods. Current use of serrapeptase supplements for infection treatment is not scientifically validated by this study.