Ethyl palmitate ameliorates lethal endotoxemia by inducing hepatic fetuin-A secretion: an
Sepsis
ethyl palmitate (EP)
fetuin-A
lipopolysaccharide (LPS)
macrophage polarization
Journal
Journal of thoracic disease
ISSN: 2072-1439
Titre abrégé: J Thorac Dis
Pays: China
ID NLM: 101533916
Informations de publication
Date de publication:
30 Sep 2024
30 Sep 2024
Historique:
received:
11
07
2024
accepted:
19
08
2024
medline:
24
10
2024
pubmed:
24
10
2024
entrez:
24
10
2024
Statut:
ppublish
Résumé
Ethyl palmitate (EP) is known to promote hepatic fetuin-A production and modulate inflammatory responses, but its potential role in lethal endotoxemia and sepsis remains unclear. This study investigates the plasma fetuin-A levels and further evaluates the impact of hepatic fetuin-A induced by EP on systemic inflammation and macrophage polarization in lethal endotoxemia and sepsis. Blood samples from 55 sepsis patients and 18 non-septic controls with similar age and sex ratio were collected to perform proteomic analyses and identify significantly different proteins. Serum fetuin-A levels in lipopolysaccharide (LPS) induced endotoxemia mice were assayed by enzyme-linked immunosorbent assay (ELISA). The mouse hepatocyte cell (AML-12) was exposed to different concentrations of EP. Our proteomic results revealed that the plasma fetuin-A levels were significantly decreased in sepsis patients compared with non-septic controls. Similarly, the serum fetuin-A levels were also reduced in endotoxemia mice compared with the control group. EP effectively promoted the production of fetuin-A in AML-12 cells and murine liver tissues. Subsequently, activation of fetuin-A by EP dramatically reduced LPS-induced murine mortality, alleviated lung and liver injury, down-regulated pro-inflammatory mediators and macrophage infiltration. Furthermore, EP regulated macrophage polarization from the M1 (CD45 EP-induced production of fetuin-A prevents sepsis and endotoxemia progression by promoting M2 polarization of macrophages.
Sections du résumé
Background
UNASSIGNED
Ethyl palmitate (EP) is known to promote hepatic fetuin-A production and modulate inflammatory responses, but its potential role in lethal endotoxemia and sepsis remains unclear. This study investigates the plasma fetuin-A levels and further evaluates the impact of hepatic fetuin-A induced by EP on systemic inflammation and macrophage polarization in lethal endotoxemia and sepsis.
Methods
UNASSIGNED
Blood samples from 55 sepsis patients and 18 non-septic controls with similar age and sex ratio were collected to perform proteomic analyses and identify significantly different proteins. Serum fetuin-A levels in lipopolysaccharide (LPS) induced endotoxemia mice were assayed by enzyme-linked immunosorbent assay (ELISA). The mouse hepatocyte cell (AML-12) was exposed to different concentrations of EP.
Results
UNASSIGNED
Our proteomic results revealed that the plasma fetuin-A levels were significantly decreased in sepsis patients compared with non-septic controls. Similarly, the serum fetuin-A levels were also reduced in endotoxemia mice compared with the control group. EP effectively promoted the production of fetuin-A in AML-12 cells and murine liver tissues. Subsequently, activation of fetuin-A by EP dramatically reduced LPS-induced murine mortality, alleviated lung and liver injury, down-regulated pro-inflammatory mediators and macrophage infiltration. Furthermore, EP regulated macrophage polarization from the M1 (CD45
Conclusions
UNASSIGNED
EP-induced production of fetuin-A prevents sepsis and endotoxemia progression by promoting M2 polarization of macrophages.
Identifiants
pubmed: 39444871
doi: 10.21037/jtd-24-1098
pii: jtd-16-09-6024
pmc: PMC11494534
doi:
Types de publication
Journal Article
Langues
eng
Pagination
6024-6036Informations de copyright
2024 AME Publishing Company. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-1098/coif). M.Z. serves as an unpaid editorial board member of Journal of Thoracic Disease from June 2024 to June 2026. The other authors have no conflicts of interest to declare.