Investigation of Skin Using a Mouse Model

Wound repair is a fundamental physiological process to keep the integrity of the skin, and its dysregulation results in diseases, such as chronic nonhealing wounds or excessive scarring. To study the underlying cellular and molecular mechanisms and identify new therapeutic targets, animal models are often used in the wound healing research. In this chapter, we describe an easy step-by-step protocol to generate skin wounds in a mouse model. Briefly, two full-thickness wounds extending through the panniculus carnosus are made on the dorsum on each side of the midline of a mouse, which is followed by monitoring and quantifying the wound closure. Moreover, the biopsy tissues of skin and wound-edges are collected at different time points for subsequent histology and gene expression analysis

Immunology of Wound Healing

PURPOSE OF REVIEW: Chronic wounds are a tremendous burden on the healthcare system and lead to significant patient morbidity and mortality. Normal cutaneous wound healing occurs through an intricate and delicate interplay between the immune system, keratinocytes, and dermal cells. Each cell type contributes signals that drive the normal phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This paper reviews how various immunological cell types and signaling molecules influence the way wounds develop, persist, and heal. RECENT FINDINGS: Concurrent with the achievement of hemostasis, neutrophils are the first cells to migrate to the wound bed, brought in by pro-inflammatory signals including IL-8. Their apoptosis and engulfment by macrophages (efferocytosis) provides a key signal to the local immune milieu, including macrophages, to transition to an anti-inflammatory, pro-repair state, where angiogenesis occurs and granulation tissue is laid down. Myofibroblasts, activated through contractile forces and signaling molecules, then drive remodeling, where granulation tissue becomes scar. Unchecked inflammation at this stage can result in abnormal scar formation. SUMMARY: Although the derangement of immune signals at any stage can result in impaired wound healing, recent research has shown that the key transition point lies between the inflammatory and the proliferative phases. This review summarizes the events that facilitate this transition and discusses how this process can be disrupted, leading to chronic, non-healing wounds