Critical role of tumor necrosis factor-α in the early process of wound healing in skin

Abstract

Tumor necrosis factor (TNF)-α is quickly released and initiates inflammation at wound tissues, but its precise role in wound healing is not fully understood. We examined the contribution of this cytokine to the early process of healing using a mouse model with full-thickness wounds in skin. TNF-α synthesis was detected just after wound creation, increased during the first several hours, reached a peak level on day 1, and then decreased to the basal level. In mice treated with anti-TNF-α mAb, wound closure was significantly delayed, and distances between the panniculus carnosus edges were significantly longer on day 3, compared with control. Inflammatory cell and fibroblast density were markedly decreased on day 3 in the anti-TNF-α mAb-treated mice compared with control. In contrast, wound healing was accelerated on day 3 when mice were treated with bioactive TNF-α. These results indicate that TNF-α is involved in the early process of wound healing.