Understanding wound healing in obesity

Table 1 Cytokines produced by adipose tissue that may contribute to low-grade inflammation

TNF-α	Secreted by macrophages, natural killer cells, and lymphocytes[13]. Crucial in formation and maintenance of granulomas[30]
IL-1	Produced by various cell types including macrophages, fibroblasts, and epithelial cells[13]. Stimulates fibroblast and keratinocyte growth and collagen synthesis by fibroblasts
IL-6	Secreted by various cell types including macrophages and adipocytes[13]. An important mediator of the acute phase response and regulator of glucose homeostasis in obesity
IL-8	Produced by various cell types including macrophages, epithelial cells, and endothelial cells[13]. Primarily recruits neutrophils and other granulocytes to sites of tissue injury
MCP-1	Also known as CCL2. Primarily secreted by monocytes, macrophages, and dendritic cells[13]. Attracts monocytes, memory T cells, and dendritic cells to sites of inflammation produced by either tissue injury or inflammation

TNF-α: Tumor necrosis factor alpha; IL: Interleukin; MCP-1: Monocyte chemoattractant protein-1.

Table 2 Animal models used in wound healing, advantages and disadvantages

Animal model	Advantages	Disadvantages
Hypertrophic wound model	Low cost	Hypertrophic scar different from human[27,29]
	Allows for production of hypertrophic scar[28,29]	Requires special device[28,29]
		Labor intensive: Frequent care to maintain tension and device placement[31]
Wound-induced hair follicle neogenesis (WIHN) model	Low cost
	Regeneration following adult wounding with minimal recovery of hair follicles at the scar center[32,48]	High variability: Mouse strains, environmental conditions, age of mice, and wound size)[33]
	Test therapeutics to activate regenerative wound healing[33]	May not translate to human injury[48]
Excisional wound model	Low cost	Labor intensive: Frequent dressing changes to maintain tension[35]
	Wound healing similar to human[35]
	Allows for fibroblast lineage tracing[49]