Lipidomic signatures align with inflammatory patterns and outcomes in critical illness
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Alterations in lipid metabolism have the potential to be markers as well as drivers of pathobiology of acute critical illness. Here, we took advantage of the temporal precision offered by trauma as a common cause of critical illness to identify the dynamic patterns in the circulating lipidome in critically ill humans. The major findings include an early loss of all classes of circulating lipids followed by a delayed and selective lipogenesis in patients destined to remain critically ill. The previously reported survival benefit of early thawed plasma administration was associated with preserved lipid levels that related to favorable changes in coagulation and inflammation biomarkers in causal modelling. Phosphatidylethanolamines (PE) were elevated in patients with persistent critical illness and PE levels were prognostic for worse outcomes not only in trauma but also severe COVID-19 patients. Here we show selective rise in systemic PE as a common prognostic feature of critical illness.
Originalsprog | Engelsk |
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Artikelnummer | 6789 |
Tidsskrift | Nature Communications |
Vol/bind | 13 |
Udgave nummer | 1 |
ISSN | 2041-1723 |
DOI | |
Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
This work was supported by US Army Medical Research and Materiel Command (W81XWH-12-2-0023) and National Institutes of Health (R35-GM-127027, U01HL137159, R01LM012087). We acknowledge the contribution of collaborators involved in PAMPer study for the clinical data collection. We acknowledge the contribution of Scott McCullough (Study Director, Academic - Metabolon, Inc) and Brian Ingram (Associate Director, Academic - Metabolon, Inc) for the technical support. JW was supported by Xiangya Medical School, Changsha, China. We thank Tiannan Guo and Guanghou Shui for providing public metabolomics/lipidomics dataset of COVID-19 patients.
Funding Information:
This work was supported by US Army Medical Research and Materiel Command (W81XWH-12-2-0023) and National Institutes of Health (R35-GM-127027, U01HL137159, R01LM012087). We acknowledge the contribution of collaborators involved in PAMPer study for the clinical data collection. We acknowledge the contribution of Scott McCullough (Study Director, Academic - Metabolon, Inc) and Brian Ingram (Associate Director, Academic - Metabolon, Inc) for the technical support. JW was supported by Xiangya Medical School, Changsha, China. We thank Tiannan Guo and Guanghou Shui for providing public metabolomics/lipidomics dataset of COVID-19 patients.
Publisher Copyright:
© 2022, The Author(s).
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