Chemokines in cutaneous wound healing

TLDR

Wound healing is a complex biological process involving sequential infiltration of leukocytes such as neutrophils, macrophages, mast cells, and lymphocytes that produce inflammatory and growth‑promoting cytokines. This review aims to update the roles of individual chemokines throughout the phases of cutaneous wound repair. The review examines how chemokines orchestrate inflammatory, reparative, and angiogenic processes across the distinct phases of skin wound healing. Chemokines tightly regulate leukocyte recruitment and, through receptors on resident cells, also drive epithelialization, tissue remodeling, and angiogenesis.

Abstract

Healing of wounds is one of the most complex biological events after birth as a result of the interplay of different tissue structures and a large number of resident and infiltrating cell types. The latter are mainly constituted by leukocyte subsets (neutrophils, macrophages, mast cells, and lymphocytes), which sequentially infiltrate the wound site and serve as immunological effector cells but also as sources of inflammatory and growth-promoting cytokines. Recent data demonstrate that recruitment of leukocyte subtypes is tightly regulated by chemokines. Moreover, the presence of chemokine receptors on resident cells (e.g., keratinocytes, endothelial cells) indicates that chemokines also contribute to the regulation of epithelialization, tissue remodeling, and angiogenesis. Thus, chemokines are in an exclusive position to integrate inflammatory events and reparative processes and are important modulators of human-skin wound healing. This review will focus preferentially on the role of chemokines during skin wound healing and intends to provide an update on the multiple functions of individual chemokines during the phases of wound repair.