In vitro antimicrobial activity of equine platelet lysate and mesenchymal stromal cells against common clinical pathogens
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Haileigh K Avellar1, John D Lutter1, Charan K Ganta1
1Department of Clinical Sciences (Avellar, Lutter, Beard), Department of Diagnostic Medicine/Pathobiology (Ganta, Smith, Jonnalagadda, Peloquin), College of Veterinary Medicine, Kansas State University, Manhattan, Kansas, USA; Department of Statistics, College of Arts and Sciences, Kansas State University, Manhattan, Kansas, USA (Kang, Ayub).
Abstract:
Septic arthritis is considered a medical emergency. Disease following bacterial colonization can lead to significant morbidity and mortality and requires costly treatment. Antimicrobial properties of regenerative therapies, including mesenchymal stromal cells and platelet products, have been researched extensively in human medicine. Although fewer studies have been conducted in veterinary species, they have shown promising results. The purpose of this study was to evaluate bacterial suppression by equine platelet lysate (EPL) and adipose-derived mesenchymal stromal cells (ASCs) in vitro. We hypothesized that both products would significantly inhibit the growth of Staphylococcus aureus and Escherichia coli. Pooled blood from 10 horses was used for production of EPL. Mesenchymal stromal cells were isolated from adipose tissue harvested from the gluteal region of 3 horses. The study evaluated 3 treatment groups: 10 × EPL, 1.6 million ASCs, and a control, using an incomplete unbalanced block design with repeated measurements. Optical density readings and colony-forming units/mL were calculated at 0, 3, 6, 9, 12, 18, and 24 hours. Decreased bacterial growth was seen at multiple time points for the S. aureus-ASC and S. aureus-EPL treatments, supporting our hypothesis. Increased bacterial growth was noticed in the E. coli-EPL group, with no difference in the E. coli-ASC treatment, which opposed our hypothesis. A clear conclusion of antimicrobial effects of EPL and ASCs cannot be made from this in vitro study. Although it appears that ASCs have a significant effect on decreasing the growth of S. aureus, further studies are needed to explore these effects, particularly in Gram-positive bacteria.
Insights
Equine platelet lysate (EPL) and adipose-derived mesenchymal stromal cells (ASCs) showed some ability to inhibit bacterial growth in vitro. While ASCs reduced Staphylococcus aureus growth, results for E. coli were inconclusive, requiring further research.
Area of Science:
- Veterinary regenerative medicine
- Antimicrobial therapies
- Equine medicine
Background:
- Septic arthritis is a critical condition in horses, leading to severe illness and death.
- Regenerative therapies like mesenchymal stromal cells and platelet products show antimicrobial potential.
- Limited research exists on these therapies' efficacy in veterinary species.
Purpose of the Study:
- To assess the in vitro bacterial suppression capabilities of equine platelet lysate (EPL) and adipose-derived mesenchymal stromal cells (ASCs).
- To test the hypothesis that both EPL and ASCs inhibit Staphylococcus aureus and Escherichia coli growth.
Main Methods:
- Equine platelet lysate (EPL) was produced from pooled horse blood.
- Adipose-derived mesenchymal stromal cells (ASCs) were isolated from equine adipose tissue.
- In vitro study design compared EPL, ASCs, and a control group against S. aureus and E. coli, measuring bacterial growth over 24 hours.
Main Results:
- Both S. aureus-ASC and S. aureus-EPL treatments demonstrated decreased bacterial growth.
- The E. coli-EPL group showed increased bacterial growth, while the E. coli-ASC group showed no significant difference.
- Results partially supported the hypothesis for S. aureus but not for E. coli.
Conclusions:
- This in vitro study cannot definitively conclude the antimicrobial effects of EPL and ASCs.
- ASCs may have a significant effect on reducing Staphylococcus aureus growth.
- Further research is necessary to explore the antimicrobial potential of these therapies, especially against Gram-positive bacteria.

