Hyperglycemia induces inflammatory response of human macrophages to CD163-mediated scavenging of hemoglobin-haptoglobin complexes
Hyperglycemia, a hallmark of diabetes, can induce inflammatory programming of macrophages. The macrophage scavenger receptor CD163 internalizes and degrades hemoglobin-haptoglobin (Hb-Hp) complexes built due to intravascular hemolysis. Clinical studies have demonstrated a correlation between impaire...
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| Hauptverfasser: | , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
26 January 2022
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| In: |
International journal of molecular sciences
Year: 2022, Jahrgang: 23, Heft: 3, Pages: 1-19 |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms23031385 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.3390/ijms23031385 Verlag, kostenfrei, Volltext: https://www.mdpi.com/1422-0067/23/3/1385 
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| Verfasserangaben: | Laura Matuschik, Vladimir Riabov, Christina Schmuttermaier, Tatyana Sevastyanova, Christel Weiss, Harald Klüter and Julia Kzhyshkowska |
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| 245 | 1 | 0 | |a Hyperglycemia induces inflammatory response of human macrophages to CD163-mediated scavenging of hemoglobin-haptoglobin complexes |c Laura Matuschik, Vladimir Riabov, Christina Schmuttermaier, Tatyana Sevastyanova, Christel Weiss, Harald Klüter and Julia Kzhyshkowska |
| 246 | 1 | |i Titel des übergeordneten Special issue |a Crosstalk between epigenetic and metabolic mechanisms in chronic inflammation | |
| 264 | 1 | |c 26 January 2022 | |
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| 520 | |a Hyperglycemia, a hallmark of diabetes, can induce inflammatory programming of macrophages. The macrophage scavenger receptor CD163 internalizes and degrades hemoglobin-haptoglobin (Hb-Hp) complexes built due to intravascular hemolysis. Clinical studies have demonstrated a correlation between impaired scavenging of Hb-Hp complexes via CD163 and diabetic vascular complications. Our aim was to identify whether hyperglycemia is able to amplify inflammation via Hb-Hp complex interactions with the immune system. M(IFNγ), M(IL-4), and control M0 macrophages were differentiated out of primary human monocytes in normo- (5 mM) and hyperglycemic (25 mM) conditions. CD163 gene expression was decreased 5.53 times in M(IFNγ) with a further decrease of 1.99 times in hyperglycemia. Hyperglycemia suppressed CD163 surface expression in M(IFNγ) (1.43 times). Flow cytometry demonstrated no impairment of Hb-Hp uptake in hyperglycemia. However, hyperglycemia induced an inflammatory response of M(IFNγ) to Hb-Hp1-1 and Hb-Hp2-2 uptake with different dynamics. Hb-Hp1-1 uptake stimulated IL-6 release (3.03 times) after 6 h but suppressed secretion (5.78 times) after 24 h. Contrarily, Hb-Hp2-2 uptake did not affect IL-6 release after 6h but increased secretion after 24 h (3.06 times). Our data show that hyperglycemia induces an inflammatory response of innate immune cells to Hb-Hp1-1 and Hb-Hp2-2 uptake, converting the silent Hb-Hp complex clearance that prevents vascular damage into an inflammatory process, hereby increasing the susceptibility of diabetic patients to vascular complications. | ||
| 650 | 4 | |a CD163 | |
| 650 | 4 | |a diabetes mellitus | |
| 650 | 4 | |a hemoglobin-haptoglobin complexes | |
| 650 | 4 | |a hyperglycemia | |
| 650 | 4 | |a inflammation | |
| 650 | 4 | |a macrophages | |
| 650 | 4 | |a scavenger receptor | |
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