Traumatic Brain Injury Induces Early Barrier Protective Responses in Incisional Skin Wounds Accelerating Cutaneous Wound Healing.

Abstract

Though Traumatic Brain Injury (TBI) and skin trauma often occur together, it is unresolved whether TBI changes the healing of skin wounds. We here explored whether TBI impacts the sequence of events during skin wound healing. Incisional skin wounds from mice subjected to TBI were assessed employing unbiased transcriptome analysis and immunostaining. Transcriptome analysis at day 1 after combined trauma detects a significant enrichment of genes involved in macrophage and T cell recruitment and activation in contrast to skin wounds without TBI. At day 7 after combined trauma, genes in pathways of re-epithelialisation including cornification and keratinisation and of anti-inflammatory responses were highly enriched. These findings were confirmed by immunostaining with increased re-epithelialisation and cornification and an increased number of macrophages and T cells resolving inflammation. Moreover, the number of dermal myofibroblasts is highly increased in skin wounds after combined trauma. Collectively, TBI induces a robust defence response characterised by early onset of enhanced immunity, faster epidermal barrier formation, and myofibroblast-driven acceleration of wound closure, which may together help counteract systemic infection.