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Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury

Globally, burns are a significant cause of injury that can cause substantial acute trauma as well as lead to increased incidence of chronic comorbidity and disease. To date, research has primarily focused on the systemic response to severe injury, with little in the literature reported on the impact...

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Bibliographic Details
Published in:Journal of proteome research 2024-08, Vol.23 (8), p.2893-2907
Main Authors: Ryan, Monique J., Raby, Edward, Whiley, Luke, Masuda, Reika, Lodge, Samantha, Nitschke, Philipp, Maker, Garth L., Wist, Julien, Holmes, Elaine, Wood, Fiona M., Nicholson, Jeremy K., Fear, Mark W., Gray, Nicola
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Language:English
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Summary:Globally, burns are a significant cause of injury that can cause substantial acute trauma as well as lead to increased incidence of chronic comorbidity and disease. To date, research has primarily focused on the systemic response to severe injury, with little in the literature reported on the impact of nonsevere injuries ( 6.83e–1) and monoacyglyceride (20:4) (p-value < 1.0e–4) and decreases in circulating anti-inflammatory high-density lipoprotein-4 subfractions (VIP > 7.75e–1), phosphatidylcholines, phosphatidylglycerols, phosphatidylinositols, and phosphatidylserines. The results indicate a persistent systemic metabolic phenotype that occurs even in cases of a nonsevere burn injury. The phenotype is indicative of an acute inflammatory profile that continues to be sustained postinjury, suggesting an impact on systems health beyond the site of injury. The phenotypes contained metabolic signatures consistent with chronic inflammatory states reported to have an elevated incidence postburn injury. Such phenotypic signatures may provide patient stratification opportunities, to identify individual responses to injury, personalize intervention strategies, and improve acute care, reducing the risk of chronic comorbidity.
ISSN:1535-3893
1535-3907
1535-3907
DOI:10.1021/acs.jproteome.3c00516