Abstract
The timely resolution of wound healing is critical for restoring the skin as a protective barrier. The switch from a proinflammatory to a reparative microenvironment must be tightly regulated. Interleukin (IL)-6 is a key modulator of the inflammatory and reparative process: it is involved in the differentiation, activation, and proliferation of leukocytes, endothelial cells, keratinocytes, and fibroblasts. This review examines the role of IL-6 in the healing of cutaneous wounds, and how dysregulation of IL-6 signaling can lead to either fibrosis or a failure to heal. The role of an IL-6/TGF-β feedback loop is discussed in the context of fibrogenesis, while IL-6 expression and responses in advanced age, diabetes, and obesity is outlined regarding the development of chronic wounds. Current research on therapies that modulate IL-6 is explored. Here, we consider IL-6′s diverse impact on cutaneous wound healing.
Highlights
Interleukin (IL)-6 plays a central role in acute inflammation and is necessary for the timely resolution of wound healing [1,2]
The role of IL-6 in the healing of cutaneous wounds cannot be understated, and the timing of the inflammatory response is paramount to a successful resolution and wound closure, where impairment of the IL-6 signaling pathway delays wound healing
The IL-6/TGF-β feedback loop is implicated in the pathogenesis of several profibrotic skin conditions, as it operates in a positive autocrine loop in fibroblasts, bolstered by IL-17A, to increase collagen deposition and the differentiation of fibroblasts to myofibroblasts, which contract to pull the edges of a wound together
Summary
Interleukin (IL)-6 plays a central role in acute inflammation and is necessary for the timely resolution of wound healing [1,2]. IL-6 signaling is responsible for the switch to a reparative environment. If the switch to proliferative signaling is not carefully controlled, repair can instead result in fibrosis, which is characterized by the excessive accumulation of extracellular matrix proteins, such as collagen, at the site of injury/damage. Scar formation is the normal end point of mammalian tissue repair, excessive scarring can impair normal tissue function [10]. Fibrotic skin tissue covers a spectrum of severity, from flat and pale and relatively static atrophic scars to severe, highly pigmented and rapidly growing pathological hypertrophic and keloid scars [11]. We will explore how IL-6 mediates the process of dermal wound repair, and the mechanisms by which it can lead to skin pathology.
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