Leukocyte presence does not increase microbicidal activity of Platelet-rich Plasma in vitro

Erminia Mariani1,2, Valentina Canella3, Andrea Berlingeri4

  • 1Laboratory of Immunorheumatology and Tissue Regeneration/RAMSES, Rizzoli Orthopaedic Institute, Via di Barbiano 1/10, 40136, Bologna, Italy. erminia.mariani@unibo.it.

BMC Microbiology
|July 31, 2015
PubMed
Abstract

Insights

Platelet-rich plasma (PRP) exhibits antibacterial properties, with leukocyte-enriched PRP (L-PRP) and pure PRP (P-PRP) showing similar effectiveness. Cryopreservation of L-PRP maintains its microbicidal activity, and new antimicrobial proteins were identified.

Area of Science:

  • Biomedical Science
  • Immunology
  • Microbiology

Background:

  • Human platelets contain molecules with regenerative and microbicidal properties.
  • Platelet-rich plasma (PRP) concentrates these molecules, potentially enhanced by leukocytes.
  • Limited research exists on PRP's true microbicidal potential.

Purpose of the Study:

  • To compare the in vitro microbicidal activity of leukocyte-enriched PRP (L-PRP) and pure PRP (P-PRP).
  • To assess the contribution of leukocytes to PRP's microbicidal properties.
  • To evaluate the effect of cryopreservation on L-PRP's microbicidal effectiveness.

Main Methods:

  • In vitro testing of P-PRP and L-PRP against common bacterial pathogens (E. coli, S. aureus, K. pneumoniae, P. aeruginosa, E. faecalis).
  • Evaluation of cryopreserved L-PRP (L-PRP cryo).
  • Analysis of microbicidal proteins released by the preparations.

Main Results:

  • L-PRP, L-PRP cryo, and P-PRP demonstrated comparable bacterial growth inhibition (1-4 log) up to 4 hours.
  • Several proteins, including MIP-1α, RANTES, GRO-α, IL-8, NAP-2, SDF-1α, and IL-6, exhibited strong microbicidal potential.

Conclusions:

  • Both L-PRP and P-PRP possess in vitro antibacterial activity.
  • Cryopreservation of L-PRP does not significantly alter its effectiveness.
  • Leukocytes do not appear to be essential for PRP's microbicidal activity, with NAP-2, SDF-1α, and IL-6 identified as key contributors.