Antimicrobial peptides are essential to innate host defense as effectors of pathogen clearance and can modify host cell behaviors to promote
wound repair. While these two functions appear interrelated, it is unclear whether the ability to aid in
wound repair requires inherent antimicrobial function. We hypothesized that the influence of
antimicrobial peptides on
wound repair is not dependent on antimicrobial function. To explore this, we analyzed the microbial killing activity of
peptide fragments and correlated this with the ability to influence
wound repair in mice. HB-107, a
peptide lacking antimicrobial activity and originally derived from the antimicrobial
cecropin B, showed up to 64 percent improvement in
wound repair compared to scrambled
peptide and vehicle controls, an effect comparable to treatment with recombinant human
platelet-derived growth factor-BB (formulated as
Regranex).
Wounds treated with HB-107 showed keratinocyte
hyperplasia and increased leukocyte infiltration. Furthermore, HB-107 stimulated
interleukin-8 secretion from cultured endothelial cells, an effect that may explain the increase in leukocyte migration. These findings confirm that
antimicrobial peptides can function as effectors of cutaneous
wound repair. Moreover, this study furthers our understanding of
antimicrobial peptides by showing that their
wound repair properties can be independent of antimicrobial function.