RvE1 Attenuates Polymicrobial Sepsis-Induced Cardiac Dysfunction and Enhances Bacterial Clearance.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2020
Historique:
received: 24 06 2020
accepted: 30 07 2020
entrez: 28 9 2020
pubmed: 29 9 2020
medline: 23 4 2021
Statut: epublish

Résumé

The development of cardiac dysfunction caused by microbial infection predicts high mortality in sepsis patients. Specialized pro-resolving mediators (SPMs) mediate resolution of inflammation in many inflammatory diseases, and are differentially expressed in plasma of sepsis patients. Here, we investigated whether the levels of SPMs are altered in the murine septic heart following polymicrobial sepsis-induced cardiac dysfunction. Ten weeks-old male C57BL/6 mice were subjected to polymicrobial sepsis induced by cecal ligation and puncture (CLP), which is a clinically relevant sepsis model receiving analgesics, antibiotics, and fluid resuscitation. CLP caused a significant systolic dysfunction assessed by echocardiography. The hearts were subjected to LC-MS/MS based lipid mediator profiling. Many SPMs were significantly reduced in septic hearts, among which RvE1 had a ~93-fold reduction. Treatment of CLP mice with synthetic RvE1 (1 μg/mouse

Identifiants

pubmed: 32983159
doi: 10.3389/fimmu.2020.02080
pmc: PMC7492649
doi:

Substances chimiques

Biomarkers 0
Inflammation Mediators 0
Eicosapentaenoic Acid AAN7QOV9EA
5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid GND3JH08JA

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2080

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 107613/Z/15/Z
Pays : United Kingdom

Informations de copyright

Copyright © 2020 Chen, Purvis, Collotta, Al Zoubi, Sugimoto, Cacace, Martin, Colas, Collino, Dalli and Thiemermann.

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Auteurs

Jianmin Chen (J)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.

Gareth S D Purvis (GSD)

Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.

Debora Collotta (D)

Department of Drug Science and Technology, University of Turin, Turin, Italy.

Sura Al Zoubi (S)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
Department of Basic Medical Sciences, School of Medicine, Al-Balqa Applied University, As-Salt, Jordan.

Michelle A Sugimoto (MA)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.

Antonino Cacace (A)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
Diabetes Complication Research Centre, School of Medicine, UCD Conway Institute, University College Dublin, Dublin, Ireland.

Lukas Martin (L)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
Department of Intensive Care and Intermediate Care, RWTH University Hospital Aachen, Aachen, Germany.

Roman A Colas (RA)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.

Massimo Collino (M)

Department of Drug Science and Technology, University of Turin, Turin, Italy.

Jesmond Dalli (J)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.

Christoph Thiemermann (C)

Barts and the London School of Medicine and Dentistry, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.

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Classifications MeSH