Imperial College London
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Dr Evangelos Triantafyllou

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Lecturer in Liver Immunology
 
 
 
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Contact

 

e.triantafyllou Website

 
 
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Location

 

10.N12ACommonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@inproceedings{Trovato:2021:10.1002/hep.31738,
author = {Trovato, FM and Zia, R and Napoli, S and Wolfer, K and Huang, X and Morgan, PE and Husbyn, H and Elgosbi, M and Lucangeli, M and Miquel, R and Wilson, I and Heaton, ND and Heneghan, MA and Auzinger, G and Antoniades, CG and Wendon, JA and Patel, VC and Coen, M and Triantafyllou, E and McPhail, MJ},
doi = {10.1002/hep.31738},
pages = {907--925},
publisher = {Ovid Technologies (Wolters Kluwer Health)},
title = {Dysregulation of the Lysophosphatidylcholine/Autotaxin/Lysophosphatidic Acid Axis in AcuteonChronic Liver Failure Is Associated With Mortality and Systemic Inflammation by Lysophosphatidic Acid–Dependent Monocyte Activation},
url = {http://dx.doi.org/10.1002/hep.31738},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - CPAPER
AB  - <jats:sec>            <jats:title>Background & Aims</jats:title>            <jats:p>Acuteonchronic liver failure (ACLF) is characterized by systemic inflammation, monocyte dysfunction, and susceptibility to infection. Lysophosphatidylcholines (LPCs) are immuneactive lipids whose metabolic regulation and effect on monocyte function in ACLF is open for study.</jats:p>          </jats:sec>          <jats:sec>            <jats:title>Approaches & Results</jats:title>            <jats:p>Three hundred fortytwo subjects were recruited and characterized for blood lipid, cytokines, phospholipase (PLA), and autotaxin (ATX) concentration. Peripheral blood mononuclear cells and CD14<jats:sup>+</jats:sup> monocytes were cultured with LPC, or its autotaxin (ATX)derived product, lysophosphatidic acid (LPA), with or without lipopolysaccharide stimulation and assessed for surface marker phenotype, cytokines production, ATX and LPAreceptor expression, and phagocytosis. Hepatic ATX expression was determined by immunohistochemistry. Healthy volunteers and patients with sepsis or acute liver failure served as controls. ACLF serum was depleted in LPCs with upregulated LPA levels. Patients who died had lower LPC levels than survivors (area under the receiver operating characteristic curve, 0.94; <jats:italic toggle="yes">P</jats:italic> < 0.001). Patients with highgrade ACLF had the lowest LPC concentrations and these rose over the first 3 days of admission. ATX concentrations were higher in patients with AD and ACLF and correlated with Model for EndStage Liver Disease, Consortium on Chronic Liver Failure–Sequential Organ Failure Assessment, and LPC/LPA concentrations. Reduction in LPC correlated with higher monocyte Mertyrosinekinase (MerTK) and CD163 expression. Plasma ATX concentrations rose dynamically during ACLF evolution, correlating wi
AU  - Trovato,FM
AU  - Zia,R
AU  - Napoli,S
AU  - Wolfer,K
AU  - Huang,X
AU  - Morgan,PE
AU  - Husbyn,H
AU  - Elgosbi,M
AU  - Lucangeli,M
AU  - Miquel,R
AU  - Wilson,I
AU  - Heaton,ND
AU  - Heneghan,MA
AU  - Auzinger,G
AU  - Antoniades,CG
AU  - Wendon,JA
AU  - Patel,VC
AU  - Coen,M
AU  - Triantafyllou,E
AU  - McPhail,MJ
DO  - 10.1002/hep.31738
EP  - 925
PB  - Ovid Technologies (Wolters Kluwer Health)
PY  - 2021///
SN  - 0270-9139
SP  - 907
TI  - Dysregulation of the Lysophosphatidylcholine/Autotaxin/Lysophosphatidic Acid Axis in AcuteonChronic Liver Failure Is Associated With Mortality and Systemic Inflammation by Lysophosphatidic Acid–Dependent Monocyte Activation
UR  - http://dx.doi.org/10.1002/hep.31738
ER  -
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