HIF-1α regulates IL-1β and IL-17 in sarcoidosis
Identifieur interne : 000519 ( Ncbi/Checkpoint ); précédent : 000518; suivant : 000520HIF-1α regulates IL-1β and IL-17 in sarcoidosis
Auteurs : Jaya Talreja [États-Unis] ; Harvinder Talwar [États-Unis] ; Christian Bauerfeld [États-Unis] ; Lawrence I. Grossman [États-Unis] ; Kezhong Zhang [États-Unis] ; Paul Tranchida [États-Unis] ; Lobelia Samavati [États-Unis]Source :
- eLife [ 2050-084X ] ; ????.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Cellules Th17 (immunologie), Femelle, Humains, Inflammation (anatomopathologie), Interleukine-1 bêta (biosynthèse), Interleukine-17 (biosynthèse), Jeune adulte, Lymphocytes auxiliaires Th1 (immunologie), Macrophages (anatomopathologie), Monocytes (anatomopathologie), Mâle, Poumon (anatomopathologie), Régulation de l'expression des gènes, Sarcoïdose (anatomopathologie), Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme).
- MESH :
- anatomopathologie : Inflammation, Macrophages, Monocytes, Poumon, Sarcoïdose.
- biosynthèse : Interleukine-1 bêta, Interleukine-17.
- immunologie : Cellules Th17, Lymphocytes auxiliaires Th1.
- métabolisme : Sous-unité alpha du facteur-1 induit par l'hypoxie.
- Adolescent, Adulte, Femelle, Humains, Jeune adulte, Mâle, Régulation de l'expression des gènes.
English descriptors
- KwdEn :
- Adolescent, Adult, Female, Gene Expression Regulation, Humans, Hypoxia-Inducible Factor 1, alpha Subunit (metabolism), Inflammation (pathology), Interleukin-17 (biosynthesis), Interleukin-1beta (biosynthesis), Lung (pathology), Macrophages (pathology), Male, Monocytes (pathology), Sarcoidosis (pathology), Th1 Cells (immunology), Th17 Cells (immunology), Young Adult.
- MESH :
- chemical , biosynthesis : Interleukin-17, Interleukin-1beta.
- chemical , metabolism : Hypoxia-Inducible Factor 1, alpha Subunit.
- immunology : Th1 Cells, Th17 Cells.
- pathology : Inflammation, Lung, Macrophages, Monocytes, Sarcoidosis.
- Adolescent, Adult, Female, Gene Expression Regulation, Humans, Male, Young Adult.
Abstract
Sarcoidosis is a complex systemic granulomatous disease of unknown etiology characterized by the presence of activated macrophages and Th1/Th17 effector cells. Data mining of our RNA-Seq analysis of CD14+monocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis. Further investigation revealed that sarcoidosis macrophages and monocytes exhibit higher protein levels for HIF-α isoforms, HIF-1β, and their transcriptional co-activator p300 as well as glucose transporter 1 (Glut1). In situ hybridization of sarcoidosis granulomatous lung tissues showed abundance of HIF-1α in the center of granulomas. The abundance of HIF isoforms was mechanistically linked to elevated IL-1β and IL-17 since targeted down regulation of HIF-1α via short interfering RNA or a HIF-1α inhibitor decreased their production. Pharmacological intervention using chloroquine, a lysosomal inhibitor, decreased lysosomal associated protein 2 (LAMP2) and HIF-1α levels and modified cytokine production. These data suggest that increased activity of HIF-α isoforms regulate Th1/Th17 mediated inflammation in sarcoidosis.
Url:
DOI: 10.7554/eLife.44519
PubMed: 30946009
PubMed Central: 6506207
Affiliations:
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PMC:6506207Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Sarcoidosis is a complex systemic granulomatous disease of unknown etiology characterized by the presence of activated macrophages and Th1/Th17 effector cells. Data mining of our RNA-Seq analysis of CD14<sup>+</sup>
monocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis. Further investigation revealed that sarcoidosis macrophages and monocytes exhibit higher protein levels for HIF-α isoforms, HIF-1β, and their transcriptional co-activator p300 as well as glucose transporter 1 (Glut1). In situ hybridization of sarcoidosis granulomatous lung tissues showed abundance of HIF-1α in the center of granulomas. The abundance of HIF isoforms was mechanistically linked to elevated IL-1β and IL-17 since targeted down regulation of HIF-1α via short interfering RNA or a HIF-1α inhibitor decreased their production. Pharmacological intervention using chloroquine, a lysosomal inhibitor, decreased lysosomal associated protein 2 (LAMP2) and HIF-1α levels and modified cytokine production. These data suggest that increased activity of HIF-α isoforms regulate Th1/Th17 mediated inflammation in sarcoidosis.</p>
</div>
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<tree><country name="États-Unis"><noRegion><name sortKey="Talreja, Jaya" sort="Talreja, Jaya" uniqKey="Talreja J" first="Jaya" last="Talreja">Jaya Talreja</name>
</noRegion>
<name sortKey="Bauerfeld, Christian" sort="Bauerfeld, Christian" uniqKey="Bauerfeld C" first="Christian" last="Bauerfeld">Christian Bauerfeld</name>
<name sortKey="Grossman, Lawrence I" sort="Grossman, Lawrence I" uniqKey="Grossman L" first="Lawrence I" last="Grossman">Lawrence I. Grossman</name>
<name sortKey="Samavati, Lobelia" sort="Samavati, Lobelia" uniqKey="Samavati L" first="Lobelia" last="Samavati">Lobelia Samavati</name>
<name sortKey="Talwar, Harvinder" sort="Talwar, Harvinder" uniqKey="Talwar H" first="Harvinder" last="Talwar">Harvinder Talwar</name>
<name sortKey="Tranchida, Paul" sort="Tranchida, Paul" uniqKey="Tranchida P" first="Paul" last="Tranchida">Paul Tranchida</name>
<name sortKey="Zhang, Kezhong" sort="Zhang, Kezhong" uniqKey="Zhang K" first="Kezhong" last="Zhang">Kezhong Zhang</name>
</country>
</tree>
</affiliations>
</record>
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