Inhibitory activities of platelet-rich and platelet-poor plasma on the growth- of pathogenic bacteria

Abstract

<strong><em>Background</em></strong><strong><em>:</em></strong>The utility and efficacy of novel materials in tissue regeneration and antimicrobial therapy are contingent upon the employment of either blood derivatives rich in platelets or platelet-poor-plasma (PPP). This effect is largely mediated by the increased or decreased concentration of platelets in the plasma. The current study aimed to analyze and evaluate the impact of platelet-rich (PRP) or PPP on inhibiting the growth of human pathogenic bacteria and compare their effects with those of chloramphenicol and penicillin.<br /> <strong><em>Methods</em></strong><strong>: </strong>In the current comparative study, PRP–1 was generated using 1-step blood centrifugation method; whereas, for PRP–2 and PPP the 2-step centrifugation protocol was used. The antimicrobial activity of PRP–1, 2, and PPP were tested on <em>Staphylococcus aureus</em>, <em>Escherichia coli</em>, <em>Klebsiella pneumonia</em>, <em>Pseudomonas aeruginosa</em>, <em>Streptococcus agalactiae</em>, <em>Staphylococcus epidermidis</em>, <em>Shigella </em>sp. and <em>Serratia</em> sp.Well diffusion and serial micro-dilution methods were used for this purpose. Chloramphenicol and penicillin susceptibility were tested using the disk diffusion method.<br /> <strong><em>Results</em></strong><strong>: </strong>While whole blood (WB) and PPP had no discernible impact on the growth parameters of any of the bacteria tested in the current study,PRP-1 reduced the growth rate of a few selected strains. In addition, while PRP-2 clearly inhibited the growth of <em>Shigella</em> sp.<em>, E. coli, S. aureus</em>, <em>S. agalactiae, </em>and <em>S. epidermidis</em>, it had no impact on the growth of <em>K. pneumoniae</em>, <em>P. aeruginosa,</em>and<em>Serratia </em>sp<br /> <strong><em>Conclusion</em></strong><strong>: </strong>It can be claimed that there is a strong correlation between the concentration of platelets and the antibacterial activity of PRP.