Exploring the circulating metabolome of sepsis: metabolomic and lipidomic profiles sampled in the ambulance.


Journal

Metabolomics : Official journal of the Metabolomic Society
ISSN: 1573-3890
Titre abrégé: Metabolomics
Pays: United States
ID NLM: 101274889

Informations de publication

Date de publication:
05 Oct 2024
Historique:
received: 10 06 2024
accepted: 17 09 2024
medline: 6 10 2024
pubmed: 6 10 2024
entrez: 5 10 2024
Statut: epublish

Résumé

Sepsis is defined as a dysfunctional host response to infection. The diverse clinical presentations of sepsis pose diagnostic challenges and there is a demand for enhanced diagnostic markers for sepsis as well as an understanding of the underlying pathological mechanisms involved in sepsis. From this perspective, metabolomics has emerged as a potentially valuable tool for aiding in the early identification of sepsis that could highlight key metabolic pathways and underlying pathological mechanisms. The aim of this investigation is to explore the early metabolomic and lipidomic profiles in a prospective cohort where plasma samples (n = 138) were obtained during ambulance transport among patients with infection according to clinical judgement who subsequently developed sepsis, patients who developed non-septic infection, and symptomatic controls without an infection. Multiplatform metabolomics and lipidomics were performed using UHPLC-MS/MS and UHPLC-QTOFMS. Uni- and multivariable analysis were used to identify metabolite profiles in sepsis vs symptomatic control and sepsis vs non-septic infection. Univariable analysis disclosed that out of the 457 annotated metabolites measured across three different platforms, 23 polar, 27 semipolar metabolites and 133 molecular lipids exhibited significant differences between patients who developed sepsis and symptomatic controls following correction for multiple testing. Furthermore, 84 metabolites remained significantly different between sepsis and symptomatic controls following adjustment for age, sex, and Charlson comorbidity score. Notably, no significant differences were identified in metabolites levels when comparing patients with sepsis and non-septic infection in univariable and multivariable analyses. Overall, we found that the metabolome, including the lipidome, was decreased in patients experiencing infection and sepsis, with no significant differences between the two conditions. This finding indicates that the observed metabolic profiles are shared between both infection and sepsis, rather than being exclusive to sepsis alone.

Sections du résumé

BACKGROUND BACKGROUND
Sepsis is defined as a dysfunctional host response to infection. The diverse clinical presentations of sepsis pose diagnostic challenges and there is a demand for enhanced diagnostic markers for sepsis as well as an understanding of the underlying pathological mechanisms involved in sepsis. From this perspective, metabolomics has emerged as a potentially valuable tool for aiding in the early identification of sepsis that could highlight key metabolic pathways and underlying pathological mechanisms.
OBJECTIVE OBJECTIVE
The aim of this investigation is to explore the early metabolomic and lipidomic profiles in a prospective cohort where plasma samples (n = 138) were obtained during ambulance transport among patients with infection according to clinical judgement who subsequently developed sepsis, patients who developed non-septic infection, and symptomatic controls without an infection.
METHODS METHODS
Multiplatform metabolomics and lipidomics were performed using UHPLC-MS/MS and UHPLC-QTOFMS. Uni- and multivariable analysis were used to identify metabolite profiles in sepsis vs symptomatic control and sepsis vs non-septic infection.
RESULTS RESULTS
Univariable analysis disclosed that out of the 457 annotated metabolites measured across three different platforms, 23 polar, 27 semipolar metabolites and 133 molecular lipids exhibited significant differences between patients who developed sepsis and symptomatic controls following correction for multiple testing. Furthermore, 84 metabolites remained significantly different between sepsis and symptomatic controls following adjustment for age, sex, and Charlson comorbidity score. Notably, no significant differences were identified in metabolites levels when comparing patients with sepsis and non-septic infection in univariable and multivariable analyses.
CONCLUSION CONCLUSIONS
Overall, we found that the metabolome, including the lipidome, was decreased in patients experiencing infection and sepsis, with no significant differences between the two conditions. This finding indicates that the observed metabolic profiles are shared between both infection and sepsis, rather than being exclusive to sepsis alone.

Identifiants

pubmed: 39369060
doi: 10.1007/s11306-024-02172-5
pii: 10.1007/s11306-024-02172-5
doi:

Substances chimiques

Biomarkers 0
Lipids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

111

Subventions

Organisme : Knowledge Foundation
ID : 2020-0257
Organisme : Knowledge Foundation
ID : 2018-0133
Organisme : Knowledge Foundation, Sweden
ID : 2016-0044
Organisme : Region Örebro län
ID : OLL-986200

Informations de copyright

© 2024. The Author(s).

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Auteurs

Samira Salihovic (S)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, 701 82, Örebro, Sweden.

Daniel Eklund (D)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, 701 82, Örebro, Sweden.

Robert Kruse (R)

Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, 701 82, Örebro, Sweden.
Department of Clinical Research Laboratory, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.

Ulrika Wallgren (U)

Department of Clinical Science and Education, Karolinska Institutet, Stockholm, Sweden.

Tuulia Hyötyläinen (T)

School of Science and Technology, Örebro University, Örebro, Sweden.

Eva Särndahl (E)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, 701 82, Örebro, Sweden.

Lisa Kurland (L)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. lisa.kurland@oru.se.
Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, 701 82, Örebro, Sweden. lisa.kurland@oru.se.

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