Inflammation and the regulation of repair responses in developing skin (212.2)

Abstract

Two general mechanisms exist for healing cutaneous wounds: repair and regeneration. In mature skin, injury initiates a repair process that includes periods of inflammation, cellular proliferation, and scar formation. Ideally, regeneration would occur with complete restoration of normal tissue architecture and function at the site of injury and the absence of a scar. Interestingly, a regenerative process is used to heal injured skin at early stages of development, resulting in scarless healing. However, at later stages of development, the skin heals wounds through a fibrotic repair process that leads to scar formation. Although the mechanisms involved in the switch from scarless to fibrotic healing during fetal skin development are not entirely understood, inflammation is believed to be important. Injury does not incite an inflammatory response in fetal skin early in development, whereas a strong inflammatory response is observed when fetal skin is wounded at late stages of development. We have shown that early events associated with inflammation, including mast cell activation, alarmin release, and pro‐inflammatory mediator production, contribute to the developmental differences in inflammation and healing outcomes in fetal skin. These studies could help identify novel targets for modulating inflammation, limiting scar formation, and promoting regeneration.