Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue

Abstract Adipose tissue contains a variety of immune cells, which vary in abundance and phenotype with obesity. The contribution of immune cell-derived factors to inflammatory, fibrotic and metabolic alterations in adipose tissue is not well established in human obesity. Human primary adipose tissue...

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Autores principales: Charles Caër, Christine Rouault, Tiphaine Le Roy, Christine Poitou, Judith Aron-Wisnewsky, Adriana Torcivia, Jean-Christophe Bichet, Karine Clément, Michèle Guerre-Millo, Sébastien André
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/00b226178c204eb3b6ac2e233e21710b
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spelling oai:doaj.org-article:00b226178c204eb3b6ac2e233e21710b2021-12-02T16:08:10ZImmune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue10.1038/s41598-017-02660-w2045-2322https://doaj.org/article/00b226178c204eb3b6ac2e233e21710b2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02660-whttps://doaj.org/toc/2045-2322Abstract Adipose tissue contains a variety of immune cells, which vary in abundance and phenotype with obesity. The contribution of immune cell-derived factors to inflammatory, fibrotic and metabolic alterations in adipose tissue is not well established in human obesity. Human primary adipose tissue cells, including pre-adipocytes, endothelial cells and mature adipocytes, were used to investigate deregulation of cell- and pathway-specific gene profiles. Among factors known to alter adipose tissue biology, we focus on inflammatory (IL-1β and IL-17) and pro-fibrotic (TGF-β1) factors. rIL-1β and rIL-17 induced concordant pro-inflammatory transcriptional programs in pre-adipocytes and endothelial cells, with a markedly more potent effect of IL-1β than IL-17. None of these cytokines had significant effect on fibrogenesis-related gene expression, contrasting with rTGF-β1-induced up-regulation of extracellular matrix components and pro-fibrotic factors. In mature adipocytes, all three factors promoted down-regulation of genes functionally involved in lipid storage and release. IL-1β and IL-17 impacted adipocyte metabolic genes in relation with their respective pro-inflammatory capacity, while the effect of TGF-β1 occurred in face of an anti-inflammatory signature. These data revealed that IL-1β and IL-17 had virtually no effect on pro-fibrotic alterations but promote inflammation and metabolic dysfunction in human adipose tissue, with a prominent role for IL-1β.Charles CaërChristine RouaultTiphaine Le RoyChristine PoitouJudith Aron-WisnewskyAdriana TorciviaJean-Christophe BichetKarine ClémentMichèle Guerre-MilloSébastien AndréNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Charles Caër
Christine Rouault
Tiphaine Le Roy
Christine Poitou
Judith Aron-Wisnewsky
Adriana Torcivia
Jean-Christophe Bichet
Karine Clément
Michèle Guerre-Millo
Sébastien André
Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
description Abstract Adipose tissue contains a variety of immune cells, which vary in abundance and phenotype with obesity. The contribution of immune cell-derived factors to inflammatory, fibrotic and metabolic alterations in adipose tissue is not well established in human obesity. Human primary adipose tissue cells, including pre-adipocytes, endothelial cells and mature adipocytes, were used to investigate deregulation of cell- and pathway-specific gene profiles. Among factors known to alter adipose tissue biology, we focus on inflammatory (IL-1β and IL-17) and pro-fibrotic (TGF-β1) factors. rIL-1β and rIL-17 induced concordant pro-inflammatory transcriptional programs in pre-adipocytes and endothelial cells, with a markedly more potent effect of IL-1β than IL-17. None of these cytokines had significant effect on fibrogenesis-related gene expression, contrasting with rTGF-β1-induced up-regulation of extracellular matrix components and pro-fibrotic factors. In mature adipocytes, all three factors promoted down-regulation of genes functionally involved in lipid storage and release. IL-1β and IL-17 impacted adipocyte metabolic genes in relation with their respective pro-inflammatory capacity, while the effect of TGF-β1 occurred in face of an anti-inflammatory signature. These data revealed that IL-1β and IL-17 had virtually no effect on pro-fibrotic alterations but promote inflammation and metabolic dysfunction in human adipose tissue, with a prominent role for IL-1β.
format article
author Charles Caër
Christine Rouault
Tiphaine Le Roy
Christine Poitou
Judith Aron-Wisnewsky
Adriana Torcivia
Jean-Christophe Bichet
Karine Clément
Michèle Guerre-Millo
Sébastien André
author_facet Charles Caër
Christine Rouault
Tiphaine Le Roy
Christine Poitou
Judith Aron-Wisnewsky
Adriana Torcivia
Jean-Christophe Bichet
Karine Clément
Michèle Guerre-Millo
Sébastien André
author_sort Charles Caër
title Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
title_short Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
title_full Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
title_fullStr Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
title_full_unstemmed Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
title_sort immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/00b226178c204eb3b6ac2e233e21710b
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