The Role of IL-13 and IL-4 in Adipose Tissue Fibrosis

White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases....

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Published inInternational journal of molecular sciences Vol. 24; no. 6; p. 5672
Main Authors Arndt, Lilli, Lindhorst, Andreas, Neugebauer, Julia, Hoffmann, Anne, Hobusch, Constance, Alexaki, Vasileia-Ismini, Ghosh, Adhideb, Blüher, Matthias, Wolfrum, Christian, Glaß, Markus, Gericke, Martin
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.03.2023
MDPI
Subjects
Actin
Adipocytes
Adipose tissue
Adipose Tissue - pathology
Adipose Tissue, White - pathology
Adipose tissues
Analysis
Animals
B cells
Bisphosphonates
Body fat
Clodronic acid
Collagen
Correlation analysis
Cytokines
Depletion
Extracellular matrix
Fibroblasts
Fibronectin
Fibronectins
Fibrosis
Genetic aspects
Genotype & phenotype
Humans
IL-13
IL-4
Inflammation
Interleukin 13
Interleukin 4
Interleukin-13 - genetics
Interleukin-4 - genetics
Interleukins
Lipids
Macrophages
Metabolism
Mice
Obesity
Pathogenesis
Phenotypes
Scientific equipment and supplies industry
Smooth muscle
Type 2 diabetes
United States
Massachusetts
Germany
IL-4
adipose tissue
macrophages
fibrosis
IL-13
obesity
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Abstract White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking , which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas and correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated.
AbstractList White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking il4ra, which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas IL13 and IL4 correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated.
White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking , which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas and correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated.
White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking il4ra , which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas IL13 and IL4 correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated.
Audience Academic
Author Alexaki, Vasileia-Ismini
Hoffmann, Anne
Ghosh, Adhideb
Wolfrum, Christian
Neugebauer, Julia
Gericke, Martin
Arndt, Lilli
Hobusch, Constance
Blüher, Matthias
Lindhorst, Andreas
Glaß, Markus
AuthorAffiliation 4 Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Dresden, 01307 Dresden, Germany
2 Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Wittenberg, 06108 Halle (Saale), Germany
1 Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany
7 Institute of Molecular Medicine, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany
5 Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland
3 Helmholtz Institute for Metabolic, Obesity and Vascular Research, 04103 Leipzig, Germany
6 Functional Genomics Center Zurich, ETH Zurich and University of Zurich, 8057 Zurich, Switzerland
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Issue 6
Keywords IL-4
adipose tissue
macrophages
fibrosis
IL-13
obesity
Language English
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Snippet White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and...
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SubjectTerms Actin
Adipocytes
Adipose tissue
Adipose Tissue - pathology
Adipose Tissue, White - pathology
Adipose tissues
Analysis
Animals
B cells
Bisphosphonates
Body fat
Clodronic acid
Collagen
Correlation analysis
Cytokines
Depletion
Extracellular matrix
Fibroblasts
Fibronectin
Fibronectins
Fibrosis
Genetic aspects
Genotype & phenotype
Humans
IL-13
IL-4
Inflammation
Interleukin 13
Interleukin 4
Interleukin-13 - genetics
Interleukin-4 - genetics
Interleukins
Lipids
Macrophages
Metabolism
Mice
Obesity
Pathogenesis
Phenotypes
Scientific equipment and supplies industry
Smooth muscle
Type 2 diabetes
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Title The Role of IL-13 and IL-4 in Adipose Tissue Fibrosis
URI https://www.ncbi.nlm.nih.gov/pubmed/36982747
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Volume 24
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