BACKGROUND: Platelet (PLT) gels exhibit antimicrobial activity useful for wound healing. The nature of the antibacterial component(s) is unknown. STUDY DESIGN AND METHODS: PLT-poor plasma (PPP), PLT-rich plasma (PRP), PLT gel (PG), and solvent/detergent-treated PLT lysate (S/D-PL) from two donors were evaluated either native or after complement heat inactivation. Materials were spiked at a 10% ratio (vol/vol) with approximately 10(7-8) colony-forming units/mL with four Gram-positive and four Gram-negative bacteria of the wound flora. Bacterial count was determined by plate assays at time of spiking and after 3 and 48 hours at 31°C. Bacteria growth inhibition tests were also performed. RESULTS: There was no viable Escherichia coli colony for 48 hours after spiking to the plasma and PLT materials from both donors, corresponding to greater than 7.51 to greater than 9.05 log inactivation. Pseudomonas aeruginosa, Klebsiella pneumoniae, and Staphylococcus aureus were inactivated (approx. 4.7, 7, and 2 log, respectively) 3 hours after spiking to PRP, PPP, or S/D-PL from the first donor but less (1.1, 4.6, and 0.2 log, respectively) in PG, before a regrowth at 48 hours in all materials. Similar data were obtained with the second donor. No plasma and PLT material had antimicrobial activity against Enterobacter cloacae, Bacillus cereus, Bacillus subtilis, and Staphylococcus epidermidis. Complement-inactivated samples had no antimicrobial activity. CONCLUSION: Plasma complement is mostly responsible for the activity of plasma and PLT biomaterials against E. coli, P. aeruginosa, K. pneumoniae, and S. aureus. Activation of the coagulation to prepare PG may reduce antimicrobial activity. These findings may help optimize the control of wound infections by blood biomaterials.
BACKGROUND: Platelet (PLT) gels exhibit antimicrobial activity useful for wound healing. The nature of the antibacterial component(s) is unknown. STUDY DESIGN AND METHODS: PLT-poor plasma (PPP), PLT-rich plasma (PRP), PLT gel (PG), and solvent/detergent-treated PLT lysate (S/D-PL) from two donors were evaluated either native or after complement heat inactivation. Materials were spiked at a 10% ratio (vol/vol) with approximately 10(7-8) colony-forming units/mL with four Gram-positive and four Gram-negative bacteria of the wound flora. Bacterial count was determined by plate assays at time of spiking and after 3 and 48 hours at 31°C. Bacteria growth inhibition tests were also performed. RESULTS: There was no viable Escherichia coli colony for 48 hours after spiking to the plasma and PLT materials from both donors, corresponding to greater than 7.51 to greater than 9.05 log inactivation. Pseudomonas aeruginosa, Klebsiella pneumoniae, and Staphylococcus aureus were inactivated (approx. 4.7, 7, and 2 log, respectively) 3 hours after spiking to PRP, PPP, or S/D-PL from the first donor but less (1.1, 4.6, and 0.2 log, respectively) in PG, before a regrowth at 48 hours in all materials. Similar data were obtained with the second donor. No plasma and PLT material had antimicrobial activity against Enterobacter cloacae, Bacillus cereus, Bacillus subtilis, and Staphylococcus epidermidis. Complement-inactivated samples had no antimicrobial activity. CONCLUSION: Plasma complement is mostly responsible for the activity of plasma and PLT biomaterials against E. coli, P. aeruginosa, K. pneumoniae, and S. aureus. Activation of the coagulation to prepare PG may reduce antimicrobial activity. These findings may help optimize the control of wound infections by blood biomaterials.
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