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From mental health to the host microbiome: Looking at the forest not just the trees in wound healing (337.1)
Author(s) -
Shupp Jeffrey,
Moffatt Lauren
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.337.1
Subject(s) - microbiome , wound healing , medicine , immune system , identification (biology) , phenotype , innate immune system , bioinformatics , immunology , biology , gene , genetics , botany
The pathophysiology of acute and chronic wounds continues to be an area of active investigation. However, little is known about the interplay between transcript and epigenomic alterations and augmentations in wound healing. Further, research is lacking in identification of genotypic signatures that may lead to customized approaches to treatment. Additionally the interplay between the endogenous and the acquired microbiome may have great impacts on wound phenotype, healing, and scarring. The prokaryotic‐host interaction may play a substantial role in determining the quality and speed of wound repair. Studies examining 57 patients after burn injury show that stress system activation contributes to burn‐related pain, itch and healing. Identification of patient specific transcript signatures may lead to early identification of problematic wounds and customizable treatment. Similarly in animals and patients exposed to stress and subsequently exhibiting symptoms of PTSD immunosuppression and perturbations in pathways relating to wound healing are consistent and persist over time. Understanding the influence of these multi‐system changes could lead to the early identification of patients that need more aggressive care in order to prevent chronic non‐healing wounds that have poor healing quality. Host prokaryotic bio‐burden is being examined to determine the cutaneous microbiome and how it is altered by traumatic wounds. Experiments in burn patients and animals examining phenotypic alterations of benign microbes after injury show that virulence factor production is altered. The resulting PAMPs and DAMPs interact directly with cutaneous cells causing an innate immune response that not only leads to augmentation in inflammatory response but induces differential regulation of multiple pathways responsible for wound healing and scar.