DEPLETION OF EOSINOPHIL INFILTRATION BY ANTI-IL-5 MONOCLONAL-ANTIBODY(TRFK-5) ACCELERATES OPEN SKIN WOUND EPITHELIAL CLOSURE

Wound healing is critical to the survival of the species after injury. Using hamsters as an experimental model, me have shown that eosinophi ls infiltrate prominently into skin mounds and that they express trans forming growth factor-alpha and -beta 1 mRNAs and proteins. We hypothe sized that eosinophils are important in mound healing, As no animal mo del is genetically deficient in eosinophils, a suitable way to test th e hypothesis is to selectively reduce and/or deplete the influx of eos inophils into the wound sites. In this study, we report that anti-inte rleukin-5 monoclonal antibody (TRFK-5) treatment can deplete eosinophi ls in cutaneous healing mounds. We found that mound closure by re-epit helialization in the experimental group Nas 4 days faster than in the control group (P < 0.01), The density of eosinophils in day-9 mounds w as significantly lower in the experimental group (P < 0.01). Wound-ass ociated eosinophils in each of the TRFK-5-treated hamsters mere deplet ed to the level comparable to unwounded hamster skin. These results de monstrate that anti-interleukin-5 monoclonal antibody treatment can ef fectively decrease eosinophil infiltration into hamster cutaneous heal ing wounds and indicate a role for eosinophils in negatively affecting wound re-epithelialization.