Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.

Polyunsaturated fatty acid (PUFA) metabolites are bioactive autoacoids that play an important role in the pathogenesis of a vast number of pathologies, including gut diseases. The induction and the resolution of inflammation depend on PUFA metabolic pathways that are favored. Therefore, understandin...

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Autores principales:	Thomas Gobbetti, Pauline Le Faouder, Justine Bertrand, Marc Dubourdeau, Elisabetta Barocelli, Nicolas Cenac, Nathalie Vergnolle
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/57cd4382afee4053a2cf1a85cf4e9669
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spelling	oai:doaj.org-article:57cd4382afee4053a2cf1a85cf4e96692021-11-18T08:54:19ZPolyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.1932-620310.1371/journal.pone.0075581https://doaj.org/article/57cd4382afee4053a2cf1a85cf4e96692013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24073272/?tool=EBIhttps://doaj.org/toc/1932-6203Polyunsaturated fatty acid (PUFA) metabolites are bioactive autoacoids that play an important role in the pathogenesis of a vast number of pathologies, including gut diseases. The induction and the resolution of inflammation depend on PUFA metabolic pathways that are favored. Therefore, understanding the profile of n-6 (eicosanoids)/n-3 (docosanoids) PUFA-derived metabolites appear to be as important as gene or protein array approaches, to uncover the molecules potentially implicated in inflammatory diseases. Using high sensitivity liquid chromatography tandem mass spectrometry, we characterized the tissue profile of PUFA metabolites in an experimental model of murine intestinal ischemia reperfusion. We identified temporal and quantitative differences in PUFA metabolite production, which correlated with inflammatory damage. Analysis revealed that early ischemia induces both pro-inflammatory and anti-inflammatory eicosanoid production. Primarily, LOX- (5/15/12/8-HETE, LTB4, LxA4) and CYP- (5, 6-EET) metabolites were produced upon ischemia, but also PGE3, and PDx. This suggests that different lipids simultaneously play a role in the induction and counterbalance of ischemic inflammatory response from its onset. COX-derived metabolites were more present from 2 to 5 hours after reperfusion, fitting with the concomitant inflammatory peaks. All metabolites were decreased 48 hours post-reperfusion except for to the pro-resolving RvE precursor 18-HEPE and the PPAR-γαμμα agonist, 15d-PGJ2. Data obtained through the pharmacological blockade of transient receptor potential vanilloid-4, which can be activated by 5, 6-EET, revealed that the endogenous activation of this receptor modulates post-ischemic intestinal inflammation. Altogether, these results demonstrate that different lipid pathways are involved in intestinal ischemia-reperfusion processes. Some metabolites, which expression is severely changed upon intestinal ischemia-reperfusion could provide novel targets and may facilitate the development of new pharmacological treatments.Thomas GobbettiPauline Le FaouderJustine BertrandMarc DubourdeauElisabetta BarocelliNicolas CenacNathalie VergnollePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 9, p e75581 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Thomas Gobbetti Pauline Le Faouder Justine Bertrand Marc Dubourdeau Elisabetta Barocelli Nicolas Cenac Nathalie Vergnolle Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
description	Polyunsaturated fatty acid (PUFA) metabolites are bioactive autoacoids that play an important role in the pathogenesis of a vast number of pathologies, including gut diseases. The induction and the resolution of inflammation depend on PUFA metabolic pathways that are favored. Therefore, understanding the profile of n-6 (eicosanoids)/n-3 (docosanoids) PUFA-derived metabolites appear to be as important as gene or protein array approaches, to uncover the molecules potentially implicated in inflammatory diseases. Using high sensitivity liquid chromatography tandem mass spectrometry, we characterized the tissue profile of PUFA metabolites in an experimental model of murine intestinal ischemia reperfusion. We identified temporal and quantitative differences in PUFA metabolite production, which correlated with inflammatory damage. Analysis revealed that early ischemia induces both pro-inflammatory and anti-inflammatory eicosanoid production. Primarily, LOX- (5/15/12/8-HETE, LTB4, LxA4) and CYP- (5, 6-EET) metabolites were produced upon ischemia, but also PGE3, and PDx. This suggests that different lipids simultaneously play a role in the induction and counterbalance of ischemic inflammatory response from its onset. COX-derived metabolites were more present from 2 to 5 hours after reperfusion, fitting with the concomitant inflammatory peaks. All metabolites were decreased 48 hours post-reperfusion except for to the pro-resolving RvE precursor 18-HEPE and the PPAR-γαμμα agonist, 15d-PGJ2. Data obtained through the pharmacological blockade of transient receptor potential vanilloid-4, which can be activated by 5, 6-EET, revealed that the endogenous activation of this receptor modulates post-ischemic intestinal inflammation. Altogether, these results demonstrate that different lipid pathways are involved in intestinal ischemia-reperfusion processes. Some metabolites, which expression is severely changed upon intestinal ischemia-reperfusion could provide novel targets and may facilitate the development of new pharmacological treatments.
format	article
author	Thomas Gobbetti Pauline Le Faouder Justine Bertrand Marc Dubourdeau Elisabetta Barocelli Nicolas Cenac Nathalie Vergnolle
author_facet	Thomas Gobbetti Pauline Le Faouder Justine Bertrand Marc Dubourdeau Elisabetta Barocelli Nicolas Cenac Nathalie Vergnolle
author_sort	Thomas Gobbetti
title	Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
title_short	Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
title_full	Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
title_fullStr	Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
title_full_unstemmed	Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
title_sort	polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/57cd4382afee4053a2cf1a85cf4e9669
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Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.

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