Wound healing in healthy individuals proceeds at an optimal rate. However, in patients, with -- e.g.-- locally impaired blood flow or diabetes, chronic
wounds develop and often become infected. Chronic
wounds mean a low quality of life for the afflicted patients, not to mention enormous costs. Rather than using recombinant
growth factors to accelerate wound healing, we employed the
toll-like receptor agonist macrophage-activating lipopeptide-2 (MALP-2) to improve the healing of full-thickness excision skin
wounds in an animal model with obese, diabetic mice. A gene array experiment suggested that
MALP-2 stimulates the release of various mediators involved in wound healing. Further data to be presented in this study will show (i) that
MALP-2 is capable of stimulating the appearance of the
monocyte chemoattractant protein-1 at the
wound site, (ii) that this leads to increased leucocyte and, in particular, macrophage infiltration and (iii) that MALP-2-treated
wounds closed 2 weeks earlier than vehicle-treated controls.
MALP-2, thus, appears to stimulate the early inflammatory process needed to set in motion the ensuing consecutive natural steps of wound healing resulting in
wound closure.