Next Article in Journal
The Effects of Matriptase Inhibition on the Inflammatory and Redox Homeostasis of Chicken Hepatic Cell Culture Models
Next Article in Special Issue
Macrophages in Health and Non-Infectious Disease
Previous Article in Journal
Ischemic Mitral Regurgitation: A Multifaceted Syndrome with Evolving Therapies
Previous Article in Special Issue
Absence of Cold-Inducible RNA-Binding Protein (CIRP) Promotes Angiogenesis and Regeneration of Ischemic Tissue by Inducing M2-Like Macrophage Polarization
 
 
Article

Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2

1
Department of Nutritional Biochemistry, Institute of Nutritional Science, University of Potsdam, D-14558 Nuthetal, Germany
2
Department of Nutritional Biochemistry, Faculty of Life Sciences: Food, Nutrition and Health, University of Bayreuth, D-95326 Kulmbach, Germany
*
Author to whom correspondence should be addressed.
The authors contributed equally to the work.
Academic Editor: David G. Alleva
Biomedicines 2021, 9(5), 449; https://doi.org/10.3390/biomedicines9050449
Received: 22 March 2021 / Revised: 10 April 2021 / Accepted: 18 April 2021 / Published: 21 April 2021
(This article belongs to the Special Issue Macrophages in Health and Non-infectious Disease 2.0)
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 E2 (PGE2) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE2 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 PGE2 synthesis. PGE2 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 PGE2 in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle. View Full-Text
Keywords: macrophages; insulin; prostaglandin E2; interleukin-8; inflammation macrophages; insulin; prostaglandin E2; interleukin-8; inflammation
Show Figures

Figure 1

MDPI and ACS Style

Henkel, J.; Klauder, J.; Statz, M.; Wohlenberg, A.-S.; Kuipers, S.; Vahrenbrink, M.; Püschel, G.P. Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2. Biomedicines 2021, 9, 449. https://doi.org/10.3390/biomedicines9050449

AMA Style

Henkel J, Klauder J, Statz M, Wohlenberg A-S, Kuipers S, Vahrenbrink M, Püschel GP. Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2. Biomedicines. 2021; 9(5):449. https://doi.org/10.3390/biomedicines9050449

Chicago/Turabian Style

Henkel, Janin, Julia Klauder, Meike Statz, Anne-Sophie Wohlenberg, Sonja Kuipers, Madita Vahrenbrink, and Gerhard Paul Püschel. 2021. "Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E2" Biomedicines 9, no. 5: 449. https://doi.org/10.3390/biomedicines9050449

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop