Deletion of a tumor necrosis superfamily gene in mice leads to impaired healing that mimics chronic wounds in humans.

Wound Repair and Regeneration : Official Publication of the Wound Healing Society [and] the European Tissue Repair Society
Melissa L PetreacaManuela M Martins-Green

Abstract

Proper healing of cutaneous wounds progresses through a series of overlapping phases. Nonhealing wounds are defective in one or more of these processes and represent a major clinical problem. A critical issue in developing treatments for chronic wounds is the paucity of animal models to study the mechanisms underlying the defects in healing. Here we show that deletion of tumor necrosis factor superfamily member 14 (TNFSF14/LIGHT) leads to impaired wounds in mice that have the characteristics of nonchronic and chronic ulcers. These wounds show: (1) excessive production of cytokines, in particular three chemokines (KC/CXCL8, MCP-1/CCL2, IP-10/CXCL10), that may be key to the abnormal initiation and resolution of inflammation; (2) defective basement membranes, explaining blood vessel leakage and disruption of dermal/epidermal interactions; and (3) granulation tissue that contains high levels of Coll III, whereas Coll I is virtually absent and does not form fibrils. We also see major differences between nonchronic and chronic wounds, with the latter populated by bacterial films and producing eotaxin, a chemokine that attracts leukocytes that combat multicellular organisms (which biofilms can be considered to be). This new mouse mode...Continue Reading

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Citations

Mar 4, 2014·Advances in Wound Care·Manuela Martins-GreenLei Wang
Jan 15, 2014·Journal of Molecular Neuroscience : MN·Dawei YeFeng Gao
Jul 3, 2015·Wound Repair and Regeneration : Official Publication of the Wound Healing Society [and] the European Tissue Repair Society·Sandeep DhallManuela Martins-Green
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Jul 20, 2021·Advanced Science·Lucas SchirmerCarsten Werner
Oct 29, 2021·The Journal of Experimental Medicine·Weifeng LiuSteven C Almo

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