Depletion of eosinophil infiltration by anti-IL-5 monoclonal antibody (TRFK-5) accelerates open skin wound epithelial closure

• Published in: The American journal of pathology Vol. 151; no. 3; pp. 813 - 819
• Main Authors: Yang, J, Torio, A, Donoff, RB, Gallagher, GT, Egan, R, Weller, PF, Wong, DT
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01.09.1997; American Society for Investigative Pathology
• Subjects: Animals; Antibodies, Monoclonal - administration & dosage; Biological and medical sciences; Cricetinae; Degeneration. Regeneration. Wound healing. Graft; Eosinophils - cytology; Eosinophils - drug effects; Eosinophils - physiology; Epithelial Cells; Epithelium - drug effects; Epithelium - physiology; Fundamental and applied biological sciences. Psychology; Injections, Intraperitoneal; Interleukin-5 - antagonists & inhibitors; Interleukin-5 - immunology; Interleukin-5 - physiology; Lymphocytes - cytology; Macrophages - cytology; Male; Mast Cells - cytology; Neutrophils - cytology; Skin - injuries; Time Factors; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Wound Healing - drug effects; Wound Healing - physiology; Cytokine; Rodentia; Granulocyte; Monoclonal antibody; Wound; Eosinophil; Pathology; Vertebrata; Experimental disease; Mammalia; Depletion; Interleukin 5; Animal; Skin; Cicatrization; Hamster; Quantitative analysis
• ISSN: 0002-9440; 1525-2191

Wound healing is critical to the survival of the species after injury. Using hamsters as an experimental model, we have shown that eosinophils infiltrate prominently into skin wounds and that they express transforming growth factor-alpha and -beta 1 mRNAs and proteins. We hypothesized that eosinophils are important in wound healing. As no animal model is genetically deficient in eosinophils, a suitable way to test the hypothesis is to selectively reduce and/or deplete the influx of eosinophils into the wound sites. In this study, we report that anti-interleukin-5 monoclonal antibody (TRFK-5) treatment can deplete eosinophils in cutaneous healing wounds. We found that wound closure by re-epithelialization in the experimental group was 4 days faster than in the control group (P < 0.01). The density of eosinophils in day-9 wounds was significantly lower in the experimental group (P < 0.01). Wound-associated eosinophils in each of the TRFK-5-treated hamsters were depleted to the level comparable to unwounded hamster skin. These results demonstrate that anti-interleukin-5 monoclonal antibody treatment can effectively decrease eosinophil infiltration into hamster cutaneous healing wounds and indicate a role for eosinophils in negatively affecting wound re-epithelialization.