Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E-2
- Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E-2 (PGE(2)) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE(2) to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE(2) synthesis. PGE(2) in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that isMacrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E-2 (PGE(2)) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE(2) to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE(2) synthesis. PGE(2) in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE(2) in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.…
Verfasserangaben: | Janin HenkelORCiDGND, Julia KlauderGND, Meike StatzGND, Anne-Sophie Wohlenberg, Sonja Kuipers, Madita Vahrenbrink, Gerhard Paul PüschelORCiDGND |
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DOI: | https://doi.org/10.3390/biomedicines9050449 |
ISSN: | 2227-9059 |
Pubmed ID: | https://pubmed.ncbi.nlm.nih.gov/33919366 |
Titel des übergeordneten Werks (Englisch): | Biomedicines |
Verlag: | MDPI |
Verlagsort: | Basel |
Publikationstyp: | Wissenschaftlicher Artikel |
Sprache: | Englisch |
Datum der Erstveröffentlichung: | 21.04.2021 |
Erscheinungsjahr: | 2021 |
Datum der Freischaltung: | 08.01.2024 |
Freies Schlagwort / Tag: | inflammation; insulin; interleukin-8; macrophages; prostaglandin E-2 |
Band: | 9 |
Ausgabe: | 5 |
Aufsatznummer: | 449 |
Seitenanzahl: | 10 |
Fördernde Institution: | Deutsche ForschungsgemeinschaftGerman Research Foundation (DFG); Open Access Publishing Fund of University of Potsdam |
Organisationseinheiten: | Fakultät für Gesundheitswissenschaften |
DDC-Klassifikation: | 5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie |
6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit | |
Publikationsweg: | Open Access / Gold Open-Access |
DOAJ gelistet | |
Lizenz (Deutsch): | CC-BY - Namensnennung 4.0 International |